Oxidative damage to DNA, proteins and other macromolecules accumulates with age and has been postulated to be a major, but not the only, type of endogenous damage leading to aging. Superoxide(O2.-), hydrogen peroxide (H2O2), and hydroxyl radical (.OH), which are mutagens produced by radiation, are also by-products of normal metabolism. Lipid peroxidation gives rise to mutagenic lipid epoxides, lipid hydroperoxides, lipid alkoxyl and peroxyl radicals, and enals ([[alpha]], ß-unsaturated aldehydes). Singlet oxygen, a high energy and mutagenic form of oxygen, can be produced by transfer of energy from light, the respiratory burst from neutrophils, or lipid peroxidation.
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Animals have numerous antioxidants defenses, but since these defenses are not perfect, some DNA is oxidized. Oxidatively damaged DNA is repaired by enzymes that excise the lesions, which are then excreted in the urine. We have developed methods to assay several of these excised damaged bases in the urine of rodents and humans almost all of which appear as the free base from repair by glycosylases. We estimate that the number of oxidative hits to DNA per cell per day is about l00,000 in the rat and about l0,000 in the human. DNA repair enzymes efficiently remove most, but not all, of the lesions formed. Oxidative lesions in DNA accumulate with age, so that by the time a rat is old (2 years) it has about two million DNA lesions per cell, which is about twice that in a young rat. Mutations also accumulate with age . For example, the somatic mutation frequency in human lymphocytes, of which the contribution of oxidative DNA lesions is unknown, is about nine times greater in elderly people than in neonates. The importance of oxidative DNA lesions in cancer and aging is underscored by the existence of specific repair glycosylases that excise these lesions from DNA. In the case of 8-hydroxy-2'-deoxyguanosine, a lesion formed from oxidative damage to guanine residues in DNA, loss of a specific glycosylase activity leads to an appreciable increase in the spontaneous mutation rate, indicating the intrinsic mutagenic potential of this DNA lesion. Many other oxidative DNA lesions are likely to be important as well.
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Mitochondrial DNA (mtDNA) from rat liver has more than ten times the level of oxidative DNA damage than does nuclear DNA from the same tissue. This increase may be due to a lack of mtDNA repair enzymes, lack of histones protecting mtDNA, and the proximity of mtDNA to oxidants generated during oxidative phosphorylation. The cell defends itself against this high rate of damage by a constant turnover of mitochondria, thus presumably removing those damaged mitochondria that produce increased oxidants. Despite this turnover, oxidative lesions appear to accumulate with age in mtDNA at a higher rate than in nuclear DNA.
Oxidative damage could also account for the mutations in mtDNA that accumulate with age
Endogenous oxidants also damage proteins. Stadtman and his colleagues have shown that the proteolytic enzymes that hydrolyze oxidized proteins are not sufficient to prevent an age-associated accumulation of oxidized proteins. In two human diseases associated with premature aging, Werner's syndrome and progeria, oxidized proteins accumulate at a much higher rate than is normal. Fluorescent age pigments, which are thought to be due in part to cross-links between protein and lipid peroxidation products, also accumulate with aging.
Showing posts with label antioxidant. Show all posts
Showing posts with label antioxidant. Show all posts
Thursday, February 7, 2008
Wednesday, February 6, 2008
Raised Glutathione Levels Help Balance Immune System
Researchers from Germany and the US have found that Glutathione can boost the natural antioxidant system of the body.
The body carries many antioxidant defense systems, but inside cells a small protein called glutathione is crucial. Glutathione is essential for the function of immune cells, which protect us from viral and bacterial infections.
In people with immune deficiency, glutathione levels fall well below the normal levels in blood and immune cells. Restoring glutathione levels to those found in healthy people is likely to help immune deficient patients.
Two studies have recently been published with research backing up the claims that Glutathione helps fight disease, one in the European Journal of Clinical Investigation, from Stig Froland in Oslo, Norway, and the other by Leonore and Leonard Herzenberg, a husband and wife team from Stanford, California. The results of their work showed that glutathione levels could indeed be restored in AIDS patients and that this may improve the outlook for these patients.
Herzenberg and colleagues conducted a clinical trial in which 31 HIV-infected patients were given daily doses of Glutathione — and 30 others were given a benign sugar pill. According to the study published in the October 1 issue of the European Journal of Clinical Investigation, those taking Glutathione had increased the amount of glutathione in their bodies to near-normal levels at the end of the two-month trial.
“The importance here is that glutathione is a central component of all cells, and glutathione deficiency is associated with poor prognosis in many, many diseases,” said Herzenberg. “What we’ve proven is that giving people Glutathione replenishes the glutathione stores.”
The authors of the report concluded that “Glutathione offers useful adjunct therapy to increase protection against oxidative stress, improve immune system function and increase detoxification of acetaminophen and other drugs. These findings suggest Glutathione therapy could be valuable in other clinical situations in which there is GSH deficiency.”
“It is important to realize that these results are the culmination of over 10 years of research.” states Frank Staal, an immunologist from Rotterdam, The Netherlands, who worked in this field for many years. “The groups of Droge and Herzenberg were the first to demonstrate that Glutathione is low in AIDS and that this defect contributes to poor immune cell function." ImmuneSupport.com
Click here for more about Glutathione and its benefits to our body.
The body carries many antioxidant defense systems, but inside cells a small protein called glutathione is crucial. Glutathione is essential for the function of immune cells, which protect us from viral and bacterial infections.
In people with immune deficiency, glutathione levels fall well below the normal levels in blood and immune cells. Restoring glutathione levels to those found in healthy people is likely to help immune deficient patients.
Two studies have recently been published with research backing up the claims that Glutathione helps fight disease, one in the European Journal of Clinical Investigation, from Stig Froland in Oslo, Norway, and the other by Leonore and Leonard Herzenberg, a husband and wife team from Stanford, California. The results of their work showed that glutathione levels could indeed be restored in AIDS patients and that this may improve the outlook for these patients.
Herzenberg and colleagues conducted a clinical trial in which 31 HIV-infected patients were given daily doses of Glutathione — and 30 others were given a benign sugar pill. According to the study published in the October 1 issue of the European Journal of Clinical Investigation, those taking Glutathione had increased the amount of glutathione in their bodies to near-normal levels at the end of the two-month trial.
“The importance here is that glutathione is a central component of all cells, and glutathione deficiency is associated with poor prognosis in many, many diseases,” said Herzenberg. “What we’ve proven is that giving people Glutathione replenishes the glutathione stores.”
The authors of the report concluded that “Glutathione offers useful adjunct therapy to increase protection against oxidative stress, improve immune system function and increase detoxification of acetaminophen and other drugs. These findings suggest Glutathione therapy could be valuable in other clinical situations in which there is GSH deficiency.”
“It is important to realize that these results are the culmination of over 10 years of research.” states Frank Staal, an immunologist from Rotterdam, The Netherlands, who worked in this field for many years. “The groups of Droge and Herzenberg were the first to demonstrate that Glutathione is low in AIDS and that this defect contributes to poor immune cell function." ImmuneSupport.com
Click here for more about Glutathione and its benefits to our body.
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Sunday, February 3, 2008
Cause of Parkinson Disease
Although Parkinson’s disease can occur from viral infections or exposure to environmental toxins, such as pesticides (gardeners and farmers are more prone to Parkinson's disease).
The causes of the majority of cases are not well known. Scientists suspect that oxidative damage to neurons in the substantia nigra could well be one of the major causes, particularly due to the depletion of the antioxidants glutathione.
People who sustain substantial head injuries face an increased risk of developing Parkinson’s disease years later.
The cause of Parkinson's disease is unknown.
Many researchers believe that several factors combined are involved: free radicals, accelerated aging, environmental toxins, and genetic predisposition.
It may be that free radicals—unstable and potentially damaging molecules that lack on electron—are involved in the degeneration of dopamine-producing cells.
Free radicals add an electron by reacting with nearby molecules in a process called oxidation, which can damage nerve cells.
Chemicals called antioxidants normally protect cells from oxidative stress and damage. If antioxidative action fails to protect dopamine-producing nerve cells, they could be damaged and, subsequently, Parkinson’s disease could develop.
Dysfunctional antioxidative mechanisms are associated with older age as well, suggesting that the acceleration of age-related changes in dopamine production may be a factor.
Exposure to an environmental toxin, such as a pesticide, that inhibits dopamine production and produces free radicals and oxidation damage may be involved.
The causes of the majority of cases are not well known. Scientists suspect that oxidative damage to neurons in the substantia nigra could well be one of the major causes, particularly due to the depletion of the antioxidants glutathione.
People who sustain substantial head injuries face an increased risk of developing Parkinson’s disease years later.
The cause of Parkinson's disease is unknown.
Many researchers believe that several factors combined are involved: free radicals, accelerated aging, environmental toxins, and genetic predisposition.
It may be that free radicals—unstable and potentially damaging molecules that lack on electron—are involved in the degeneration of dopamine-producing cells.
Free radicals add an electron by reacting with nearby molecules in a process called oxidation, which can damage nerve cells.
Chemicals called antioxidants normally protect cells from oxidative stress and damage. If antioxidative action fails to protect dopamine-producing nerve cells, they could be damaged and, subsequently, Parkinson’s disease could develop.
Dysfunctional antioxidative mechanisms are associated with older age as well, suggesting that the acceleration of age-related changes in dopamine production may be a factor.
Exposure to an environmental toxin, such as a pesticide, that inhibits dopamine production and produces free radicals and oxidation damage may be involved.
Glutathione -powerful antioxidant found within every cell
Glutathione - or L Glutathione - is a powerful antioxidant found within every cell. Glutathione plays a role in nutrient metabolism, and regulation of cellular events (including gene expression, DNA and protein synthesis, cell growth, and immune response.
This antioxidant, made from the combination of three amino acids cysteine, glutamate, and glycine, forms part of the powerful natural antioxidant glutathione peroxidase which is found in our cells.
Glutathione peroxidase plays a variety of roles in cells, including DNA synthesis and repair, metabolism of toxins and carcinogens, enhancement of the immune system, and prevention of fat oxidation.
However, glutathione is predominantly known as an antioxidant protecting our cells from damage caused by the free radical hydrogen peroxide.
Glutathione also helps the other antioxidants in cells stay in their active form.
Brain glutathione levels have been found to be lower in patients with Parkinson’s disease.
Parkinson's Disease
Parkinson’s disease is a common neurological condition afflicting about 1 percent of men and women over the age of seventy. In Parkinson’s disease, a small region in the brain, called the substantia nigra, begins to deteriorate. The neurons of the substantia nigra use the brain chemical dopamine. With the loss of dopamine, tremors begin and movement slows. Despite current drug therapies, Parkinson’s disease remains a progressive and incurable condition. Many patients with Parkinson’s disease may also suffer from age related cognitive decline or have some of the symptoms of Alzheimer’s disease.
This antioxidant, made from the combination of three amino acids cysteine, glutamate, and glycine, forms part of the powerful natural antioxidant glutathione peroxidase which is found in our cells.
Glutathione peroxidase plays a variety of roles in cells, including DNA synthesis and repair, metabolism of toxins and carcinogens, enhancement of the immune system, and prevention of fat oxidation.
However, glutathione is predominantly known as an antioxidant protecting our cells from damage caused by the free radical hydrogen peroxide.
Glutathione also helps the other antioxidants in cells stay in their active form.
Brain glutathione levels have been found to be lower in patients with Parkinson’s disease.
Parkinson's Disease
Parkinson’s disease is a common neurological condition afflicting about 1 percent of men and women over the age of seventy. In Parkinson’s disease, a small region in the brain, called the substantia nigra, begins to deteriorate. The neurons of the substantia nigra use the brain chemical dopamine. With the loss of dopamine, tremors begin and movement slows. Despite current drug therapies, Parkinson’s disease remains a progressive and incurable condition. Many patients with Parkinson’s disease may also suffer from age related cognitive decline or have some of the symptoms of Alzheimer’s disease.
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Wednesday, January 23, 2008
Milk Thistle, Silymarin
Food sources and dietary supplements that help boost glutathione levels naturally.
Milk Thistle, Silymarin
Milk thistle is a powerful antioxidant and supports the liver by preventing the depletion of glutathione. Silymarin is the active compound of milk thistle.
It is a natural liver detoxifier and protects the liver from many industrial toxins such as carbon tetrachloride, and more common agents like alcohol.
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Milk Thistle, Silymarin
Milk thistle is a powerful antioxidant and supports the liver by preventing the depletion of glutathione. Silymarin is the active compound of milk thistle.
It is a natural liver detoxifier and protects the liver from many industrial toxins such as carbon tetrachloride, and more common agents like alcohol.
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N-Acetyl-Cysteine (NAC)
Food sources and dietary supplements that help boost glutathione levels naturally.
N-Acetyl-Cysteine (NAC)
It is derived from the amino acid L-Cysteine, and acts as a precursor of glutathione.
NAC is quickly metabolized into glutathione once it enters the body.
It has been proven in numerous scientific studies and clinical trials, to boost intracellular production of glutathione, and is approved by the FDA for treatment of accetaminophen overdose.
Because of glutathione mucolytic action, NAC is commonly used in the treatment of lung diseases like cystic fibrosis, bronchitis and asthma.
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N-Acetyl-Cysteine (NAC)
It is derived from the amino acid L-Cysteine, and acts as a precursor of glutathione.
NAC is quickly metabolized into glutathione once it enters the body.
It has been proven in numerous scientific studies and clinical trials, to boost intracellular production of glutathione, and is approved by the FDA for treatment of accetaminophen overdose.
Because of glutathione mucolytic action, NAC is commonly used in the treatment of lung diseases like cystic fibrosis, bronchitis and asthma.
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Tuesday, January 22, 2008
Effect of glutathione depletion on antioxidant enzymes in the epididymis, seminal vesicles, and liver and on spermatozoa motility in the aging rat
Effect of glutathione depletion on antioxidant enzymes in the epididymis, seminal vesicles, and liver and on spermatozoa motility in the aging brown Norway rat.
by: EV Zubkova, B Robaire - Biol Reprod, Vol. 71, No. 3. (September 2004), pp. 1002-1008.
Reactive oxygen species (ROS) play a role in male infertility, where excessive amounts impair spermatozoal motility.
Epididymal antioxidant enzymes protect spermatozoa from oxidative damage in the epididymal lumen. Antioxidant secretions from the seminal vesicle protect spermatozoa after ejaculation.
As it is known that with age there is increased generation of ROS, the goals of this study were to determine how aging affects the response of antioxidant enzymes in the epididymis, seminal vesicles, and liver to l-buthionine-S,R-sulfoximine (BSO) mediated glutathione (GSH) depletion, and to examine the impact of GSH depletion on motility parameters of spermatozoa from the cauda epididymidis in young (4-mo-old) and old (21-mo-old) rats.
Levels of GSH and glutathione disulfide (GSSG), as well as activities of glutathione peroxidase, glutathione reductase, catalase, and superoxide dismutase, were measured in the caput, corpus and cauda epididymidis, seminal vesicles, and liver.
Spermatozoal motility was assessed by computer-assisted sperm analysis. Significant age-related changes in antioxidant enzyme activities were found in the liver and cauda epididymidis.
Glutathione age was most evident in the cauda epididymidis, seminal vesicles, and liver, where antioxidant enzyme activities changed significantly.
Additionally, spermatozoa motility was adversely affected after BSO treatment in both age groups, but significantly more so in older animals.
In summary, the male reproductive tissues and liver undergo age-related changes in antioxidant enzyme activities and in their response to GSH depletion.
THE MAX GXL is a PATENTED High Performance Formula which:Dramatically Raises Your Energy LevelSlows Down The Aging ProcessStrengthens Your Immune SystemFights Inflammation and Diseases of AgingImproves Athletic Performance & RecoveryDetoxify Your Body
by: EV Zubkova, B Robaire - Biol Reprod, Vol. 71, No. 3. (September 2004), pp. 1002-1008.
Reactive oxygen species (ROS) play a role in male infertility, where excessive amounts impair spermatozoal motility.
Epididymal antioxidant enzymes protect spermatozoa from oxidative damage in the epididymal lumen. Antioxidant secretions from the seminal vesicle protect spermatozoa after ejaculation.
As it is known that with age there is increased generation of ROS, the goals of this study were to determine how aging affects the response of antioxidant enzymes in the epididymis, seminal vesicles, and liver to l-buthionine-S,R-sulfoximine (BSO) mediated glutathione (GSH) depletion, and to examine the impact of GSH depletion on motility parameters of spermatozoa from the cauda epididymidis in young (4-mo-old) and old (21-mo-old) rats.
Levels of GSH and glutathione disulfide (GSSG), as well as activities of glutathione peroxidase, glutathione reductase, catalase, and superoxide dismutase, were measured in the caput, corpus and cauda epididymidis, seminal vesicles, and liver.
Spermatozoal motility was assessed by computer-assisted sperm analysis. Significant age-related changes in antioxidant enzyme activities were found in the liver and cauda epididymidis.
Glutathione age was most evident in the cauda epididymidis, seminal vesicles, and liver, where antioxidant enzyme activities changed significantly.
Additionally, spermatozoa motility was adversely affected after BSO treatment in both age groups, but significantly more so in older animals.
In summary, the male reproductive tissues and liver undergo age-related changes in antioxidant enzyme activities and in their response to GSH depletion.
THE MAX GXL is a PATENTED High Performance Formula which:Dramatically Raises Your Energy LevelSlows Down The Aging ProcessStrengthens Your Immune SystemFights Inflammation and Diseases of AgingImproves Athletic Performance & RecoveryDetoxify Your Body
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Vitamin E on glutathione-dependent enzymes
Reactive oxygen species and various electrophiles are involved in the etiology of diseases varying from cancer to cardiovascular and pulmonary disorders.
The human body is protected against damaging effects of these compounds by a wide variety of systems. An important line of defense is formed by antioxidants.
Vitamin E (consisting of various forms of tocopherols and tocotrienols) is an important fat-soluble, chain-breaking antioxidant.
Besides working as an antioxidant, this compound possesses other functions with possible physiological relevance.
The glutathione-dependent enzymes form another line of defense.
Two important enzymes in this class are the free radical reductase and glutathione S-transferases (GSTs).
The GSTs are a family of phase II detoxification enzymes. They can catalyze glutathione conjugation with various electrophiles.
In most cases the electrophiles are detoxified by this conjugation, but in some cases the electrophiles are activated.
Antioxidant do not act in isolation but form an intricate network. It is, for instance, known that vitamin E, together with glutathione (GSH) and a membrane-bound heat labile GSH-dependent factor, presumably an enzyme, can prevent damaging effects of reactive oxygen species on polyunsaturated fatty acids in biomembranes (lipid peroxidation).
This manuscript reviews the interaction between the two defense systems, vitamin E and glutathione-dependent enzymes.
On the simplest level, antioxidant such as vitamin E have protective effects on glutathione-dependent enzymes; however, we will see that reality is somewhat more complicated.
by: RI van Haaften, GR Haenen, CT Evelo, A Bast
Drug Metab Rev, Vol. 35, No. 2-3. (g 2003), pp. 215-253.
Click here for more about Glutathione and its benefits to our body.
The human body is protected against damaging effects of these compounds by a wide variety of systems. An important line of defense is formed by antioxidants.
Vitamin E (consisting of various forms of tocopherols and tocotrienols) is an important fat-soluble, chain-breaking antioxidant.
Besides working as an antioxidant, this compound possesses other functions with possible physiological relevance.
The glutathione-dependent enzymes form another line of defense.
Two important enzymes in this class are the free radical reductase and glutathione S-transferases (GSTs).
The GSTs are a family of phase II detoxification enzymes. They can catalyze glutathione conjugation with various electrophiles.
In most cases the electrophiles are detoxified by this conjugation, but in some cases the electrophiles are activated.
Antioxidant do not act in isolation but form an intricate network. It is, for instance, known that vitamin E, together with glutathione (GSH) and a membrane-bound heat labile GSH-dependent factor, presumably an enzyme, can prevent damaging effects of reactive oxygen species on polyunsaturated fatty acids in biomembranes (lipid peroxidation).
This manuscript reviews the interaction between the two defense systems, vitamin E and glutathione-dependent enzymes.
On the simplest level, antioxidant such as vitamin E have protective effects on glutathione-dependent enzymes; however, we will see that reality is somewhat more complicated.
by: RI van Haaften, GR Haenen, CT Evelo, A Bast
Drug Metab Rev, Vol. 35, No. 2-3. (g 2003), pp. 215-253.
Click here for more about Glutathione and its benefits to our body.
Monday, January 21, 2008
Types of Free Radicals
Where do free radicals come from?
• Amino Acid transport
• Cellular detoxification
• Immune system enhancement
• Enzyme activation
Types of Free Radicals
The fight against free radicals is often a tricky one. There is not a mythical, ambiguous, or singular form on free radical. Science has confirmed that there are many different types of free radicals including:
• Superoxide
• Hydrogen Peroxide
• Single Oxygen and Hydroxyl Radicals
Important Note: Not all antioxidants can sufficiently match up with all types of free radicals.
The great news about Glutathione is that regardless of the type of free radical, Glutathione has the ability to properly match up and neutralize it, thus increasing cellular protection and function
Click here for more about Glutathione and its benefits to our body.
• Amino Acid transport
• Cellular detoxification
• Immune system enhancement
• Enzyme activation
Types of Free Radicals
The fight against free radicals is often a tricky one. There is not a mythical, ambiguous, or singular form on free radical. Science has confirmed that there are many different types of free radicals including:
• Superoxide
• Hydrogen Peroxide
• Single Oxygen and Hydroxyl Radicals
Important Note: Not all antioxidants can sufficiently match up with all types of free radicals.
The great news about Glutathione is that regardless of the type of free radical, Glutathione has the ability to properly match up and neutralize it, thus increasing cellular protection and function
Click here for more about Glutathione and its benefits to our body.
Glutathione Fact 1 - produced naturally in our cells
Glutathione (GSH) is a small protein produced naturally in our cells when certain required elements are present
It functions both as an antioxidant and an antitoxin and is a major defense system against illness and aging.
Our glutathione level actually indicates our state of health and can predict longevity. Although there are more than 60,000 published papers on the beneficial effects of glutathione replacement, it is still largely ignored by mainstream medicine.
In the near future the importance of glutathione will be widely recognized because it has the ability to boost the immune system and fight off the damage of free radicals on the cells.
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
It functions both as an antioxidant and an antitoxin and is a major defense system against illness and aging.
Our glutathione level actually indicates our state of health and can predict longevity. Although there are more than 60,000 published papers on the beneficial effects of glutathione replacement, it is still largely ignored by mainstream medicine.
In the near future the importance of glutathione will be widely recognized because it has the ability to boost the immune system and fight off the damage of free radicals on the cells.
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
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Friday, January 18, 2008
Glutathione peroxidase (GSH) is your body’s most abundant natural antioxidant.
GSH protects your vision, boosts your immune system, helps turn carbohydrates into energy, and prevents the buildup of oxidized fats that may contribute to atherosclerosis.
Glutathione is a compound classified as a tripeptide made of three amino acids: cysteine, glutamic acid, and glycine. Glutathione is also found in every part of the body, especially the lungs, intestinal tract, and liver.
The body produces and stores the largest amounts of GSH in the liver, where it is used to detoxify harmful compounds so that they can be removed from the body through the bile.
The liver also supplies GSH directly to red and white blood cells in the bloodstream; it helps keep red blood and white blood cells healthy to maximize the disease-fighting power of the immune system.
Glutathione also appears to have an anti-aging affect on the body. GSH levels decline with age, and a lack of Glutathione has been shown to leave the body more vulnerable to damage by free radicals, thus speeding up oxidation (wearing down) of the body.
A Glutathione deficiency can have a devastating effect on the nervous system, causing such symptoms as lack of balance and coordination, mental disorders, and tremors.
Any illness (even a bad cold), chronic disorders such as asthma and rheumatoid arthritis, injury, or heavy exposure to pollutants can cause a GSH deficiency.
This is because your body uses more GSH when it is supporting white blood cells and ridding the body of toxins.
Glutathione is found in almost all fruits and vegetables. Acorn squash, asparagus, avocado, cantaloupe, grapefruit, okra, orange, peach, potato, spinach, strawberries, tomato, watermelon, and zucchini are all good sources of GSH. Some vegetables, such as broccoli, cabbage, Brussels sprouts, cauliflower, kale, and parsley, not only provide GSH, but also actually stimulate the body produce more of this powerful antioxidant.
Cooking destroys a lot of the Glutathione in fresh fruits and vegetables, so you can get the most GSH from these foods by eating them raw or steamed.
Eating foods high in glutamine, such as lean meats, eggs, wheat germ, and whole grains, can also stimulate the liver to produce more GSH.
There is no Recommended Dietary Allowance (RDA) for GSH, but supplements have no known harmful side effects. Glutathione supplements can be expensive, but there is some question about the body’s ability to absorb GSH efficiently in supplemental form. If you want to take GSH supplements, just make sure to take them with meals to maximize absorption.
Click here for more about Glutathione and its benefits to our body.
Glutathione is a compound classified as a tripeptide made of three amino acids: cysteine, glutamic acid, and glycine. Glutathione is also found in every part of the body, especially the lungs, intestinal tract, and liver.
The body produces and stores the largest amounts of GSH in the liver, where it is used to detoxify harmful compounds so that they can be removed from the body through the bile.
The liver also supplies GSH directly to red and white blood cells in the bloodstream; it helps keep red blood and white blood cells healthy to maximize the disease-fighting power of the immune system.
Glutathione also appears to have an anti-aging affect on the body. GSH levels decline with age, and a lack of Glutathione has been shown to leave the body more vulnerable to damage by free radicals, thus speeding up oxidation (wearing down) of the body.
A Glutathione deficiency can have a devastating effect on the nervous system, causing such symptoms as lack of balance and coordination, mental disorders, and tremors.
Any illness (even a bad cold), chronic disorders such as asthma and rheumatoid arthritis, injury, or heavy exposure to pollutants can cause a GSH deficiency.
This is because your body uses more GSH when it is supporting white blood cells and ridding the body of toxins.
Glutathione is found in almost all fruits and vegetables. Acorn squash, asparagus, avocado, cantaloupe, grapefruit, okra, orange, peach, potato, spinach, strawberries, tomato, watermelon, and zucchini are all good sources of GSH. Some vegetables, such as broccoli, cabbage, Brussels sprouts, cauliflower, kale, and parsley, not only provide GSH, but also actually stimulate the body produce more of this powerful antioxidant.
Cooking destroys a lot of the Glutathione in fresh fruits and vegetables, so you can get the most GSH from these foods by eating them raw or steamed.
Eating foods high in glutamine, such as lean meats, eggs, wheat germ, and whole grains, can also stimulate the liver to produce more GSH.
There is no Recommended Dietary Allowance (RDA) for GSH, but supplements have no known harmful side effects. Glutathione supplements can be expensive, but there is some question about the body’s ability to absorb GSH efficiently in supplemental form. If you want to take GSH supplements, just make sure to take them with meals to maximize absorption.
Click here for more about Glutathione and its benefits to our body.
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Thursday, January 17, 2008
The 3 Distinct Benefits of Naturally Produced Glutathione
Glutathione: The Master Antioxidant
Antioxidants participate directly in the destruction of reactive oxygen compounds called free radicals. These by-products of a cell’s normal function can’t be avoided, but exposure to ultraviolet radiation from the sun or other sources promotes their emergence.
Free radicals have been linked to muscle fatigue during exercise and aging.
For this reason, the body is equipped with a variety of antioxidants. Vitamins C and E are natural antioxidants but do not occur naturally in the body.
These and other antioxidants actually depend on natural glutathione to function properly.
This is why Glutathione is called “The Master Antioxidant”.
Glutathione : Food for the Immune system
Glutathione helps build your Immune system resistance and improve your chances of staying healthy.
Lymphocytes are cells of your Immune system. Glutathione is essential for lymphocytes to increase in number, produce antibodies, and function efficiently.
Glutathione: A Cellular Level Detoxifier
Our food and water sources are becoming increasingly contaminated with chemicals, as is the air that we breathe.
Supplemental Detoxifier such as Glutathione help to counter the effects of the toxins we inhale and ingest.
By physically binding to toxic compounds in cells, Glutathione helps make them soluble - and harmless. The body can then eliminate these disarmed toxins in the bile and urine.
Click here for more about Glutathione and its benefits to our body.
Antioxidants participate directly in the destruction of reactive oxygen compounds called free radicals. These by-products of a cell’s normal function can’t be avoided, but exposure to ultraviolet radiation from the sun or other sources promotes their emergence.
Free radicals have been linked to muscle fatigue during exercise and aging.
For this reason, the body is equipped with a variety of antioxidants. Vitamins C and E are natural antioxidants but do not occur naturally in the body.
These and other antioxidants actually depend on natural glutathione to function properly.
This is why Glutathione is called “The Master Antioxidant”.
Glutathione : Food for the Immune system
Glutathione helps build your Immune system resistance and improve your chances of staying healthy.
Lymphocytes are cells of your Immune system. Glutathione is essential for lymphocytes to increase in number, produce antibodies, and function efficiently.
Glutathione: A Cellular Level Detoxifier
Our food and water sources are becoming increasingly contaminated with chemicals, as is the air that we breathe.
Supplemental Detoxifier such as Glutathione help to counter the effects of the toxins we inhale and ingest.
By physically binding to toxic compounds in cells, Glutathione helps make them soluble - and harmless. The body can then eliminate these disarmed toxins in the bile and urine.
Click here for more about Glutathione and its benefits to our body.
GLUTATHIONE REDOX STATUS IN THE HUMAN CELL LINE
GLUTATHIONE REDOX STATUS IN THE HUMAN CELL LINE, A549, FOLLOWING INTRACELLULAR GLUTATHIONE DEPLETION AND EXTRACELLULAR GLUTATHIONE ADDITION
Pendergrass J. A.; Srinivasan J. V.; Clark E. P.; Kumar K. S.
The redox status of Glutathione (L-gamma-glutamyl-L-cysteinylglycine, GSH) plays an im portant role in a number of different cellular reactions including cellular oxidative stress.
Using A549 human sm all cell lung carcinoma fibroblasts, we investigated the role of exogenous GSH on the intracellular GSH/Glutathione disulfide (oxidized Glutathione, GSSG) redox ratio in GSH-depleted cells by treating with L-buthionine-(S,R)-sulfoximine (BSO).
GSH levels decreased after BSO treatment. Although BSO is a well-recognized inhibitor of GSH biosynthesis and has no known effect on GSSG reductase, surprisingly, the levels of GSSG also decreased. Incubation of control or GSH-depleted cells with exogenous GSH did not alter intracellular GSH or GSSG levels to any significant extent.
Therefore, the ratio of GSH/GSSG also was not altered significantly either in the controls or the BSO-treated cells. It appears that there m ay be cellular hom eostatic mechanisms that would maintain a constant GSH/GSSG ratio, irrespective of the changes in intracellular GSH concentration.
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Pendergrass J. A.; Srinivasan J. V.; Clark E. P.; Kumar K. S.
The redox status of Glutathione (L-gamma-glutamyl-L-cysteinylglycine, GSH) plays an im portant role in a number of different cellular reactions including cellular oxidative stress.
Using A549 human sm all cell lung carcinoma fibroblasts, we investigated the role of exogenous GSH on the intracellular GSH/Glutathione disulfide (oxidized Glutathione, GSSG) redox ratio in GSH-depleted cells by treating with L-buthionine-(S,R)-sulfoximine (BSO).
GSH levels decreased after BSO treatment. Although BSO is a well-recognized inhibitor of GSH biosynthesis and has no known effect on GSSG reductase, surprisingly, the levels of GSSG also decreased. Incubation of control or GSH-depleted cells with exogenous GSH did not alter intracellular GSH or GSSG levels to any significant extent.
Therefore, the ratio of GSH/GSSG also was not altered significantly either in the controls or the BSO-treated cells. It appears that there m ay be cellular hom eostatic mechanisms that would maintain a constant GSH/GSSG ratio, irrespective of the changes in intracellular GSH concentration.
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Chronic Alcoholism Alters Systemic and Pulmonary Glutathione Redox Status
Rationale: Previous studies have linked the development and severity of acute respiratory distress syndrome with a history of alcohol abuse. In clinical studies, this association has been centered on depletion of pulmonary Glutathione and subsequent chronic oxidant stress.
Objectives: The impact on redox potential of the plasma or pulmonary pools, however, has never been reported.
Methods: Plasma and bronchoalveolar lavage fluid were collected from otherwise healthy alcohol-dependent subjects and control subjects matched by age, sex, and smoking history.
Measurements and Main Results: Redox potential was calculated from measured reduced and oxidized Glutathione in plasma and lavage. Among subjects who did and did not smoke, lavage fluid Glutathione redox potential was more oxidized in alcohol abusers by approximately 40 mV, which was not altered by dilution. This oxidation of the airway lining fluid associated with chronic alcohol abuse was independent of smoking history. A shift by 20 mV in plasma Glutathione redox potential, however, was noted only in subjects who both abused alcohol and smoked.
Conclusions: Chronic alcoholism was associated with alveolar oxidation and, with smoking, systemic oxidation. However, systemic oxidation did not accurately reflect the dramatic alcohol-induced oxidant stress in the alveolar space.
Although there was compensation for the oxidant stress caused by smoking in control groups, the capacity to maintain a reduced environment in the alveolar space was overwhelmed in those who abused alcohol. The significant alcohol-induced chronic oxidant stress in the alveolar space and the subsequent ramifications may be an important modulator of the increased incidence and severity of acute respiratory distress syndrome in this vulnerable population.
Mary Y. Yeh1, Ellen L. Burnham2, Marc Moss2 and Lou Ann S. Brown1
Objectives: The impact on redox potential of the plasma or pulmonary pools, however, has never been reported.
Methods: Plasma and bronchoalveolar lavage fluid were collected from otherwise healthy alcohol-dependent subjects and control subjects matched by age, sex, and smoking history.
Measurements and Main Results: Redox potential was calculated from measured reduced and oxidized Glutathione in plasma and lavage. Among subjects who did and did not smoke, lavage fluid Glutathione redox potential was more oxidized in alcohol abusers by approximately 40 mV, which was not altered by dilution. This oxidation of the airway lining fluid associated with chronic alcohol abuse was independent of smoking history. A shift by 20 mV in plasma Glutathione redox potential, however, was noted only in subjects who both abused alcohol and smoked.
Conclusions: Chronic alcoholism was associated with alveolar oxidation and, with smoking, systemic oxidation. However, systemic oxidation did not accurately reflect the dramatic alcohol-induced oxidant stress in the alveolar space.
Although there was compensation for the oxidant stress caused by smoking in control groups, the capacity to maintain a reduced environment in the alveolar space was overwhelmed in those who abused alcohol. The significant alcohol-induced chronic oxidant stress in the alveolar space and the subsequent ramifications may be an important modulator of the increased incidence and severity of acute respiratory distress syndrome in this vulnerable population.
Mary Y. Yeh1, Ellen L. Burnham2, Marc Moss2 and Lou Ann S. Brown1
Glutathione redox cycle protects cultured endothelial cells against lysis by extracellularly generated hydrogen peroxide
We have examined the role of the Glutathione redox cycle as an Antioxidants defense mechanism in cultured bovine and human endothelial cells by disrupting the Glutathione redox cycle at several points.
Endothelial Glutathione reductase was selectively inhibited with 1,3-bis(chloroethyl)-1-nitrosourea (BCNU). Cellular stores of reducedGlutathione were depleted by reaction with diethylmaleate (DEM) or 1-chloro-2,4-dinitrobenzene (CDNB) or by inhibition of Glutathione synthesis with buthionine sulfoximine (BSO).
Whereas several strains of untreated bovine and human endothelial cells were resistant to lysis by enzymatically generated hydrogen peroxide, BCNU-treated cells were readily lysed in a time- and dose-dependent manner. Glucose-glucose oxidase-mediated lysis of BCNU-treated bovine endothelial cells was catalase-inhibitable and directly related to BCNU concentration and endogenous Glutathione reductase activity. Pretreatment of bovine endothelial cells with BCNU did not potentiate lysis by distilled water, calcium ionophore, lipopolysaccharide, or hypochlorous acid. Depletion of cellular reduced glutathione by reaction with DEM or CDNB or by inhibition of Glutathione synthesis by BSO also potentiated endothelial lysis by enzymatically generated hydrogen peroxide. Inhibition of endothelial Glutathione reductase by BCNU or depletion of reduced glutathione by BSO increased endothelial susceptibility to lysis by hydrogen peroxide generated by phorbol myristate acetate-activated neutrophils.
We conclude that the Glutathione redox cycle plays an important role as an endogenous Antioxidants defense mechanism in cultured endothelial cells
M Harlan, J D Levine, K S Callahan, B R Schwartz, and L A Harker
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Endothelial Glutathione reductase was selectively inhibited with 1,3-bis(chloroethyl)-1-nitrosourea (BCNU). Cellular stores of reducedGlutathione were depleted by reaction with diethylmaleate (DEM) or 1-chloro-2,4-dinitrobenzene (CDNB) or by inhibition of Glutathione synthesis with buthionine sulfoximine (BSO).
Whereas several strains of untreated bovine and human endothelial cells were resistant to lysis by enzymatically generated hydrogen peroxide, BCNU-treated cells were readily lysed in a time- and dose-dependent manner. Glucose-glucose oxidase-mediated lysis of BCNU-treated bovine endothelial cells was catalase-inhibitable and directly related to BCNU concentration and endogenous Glutathione reductase activity. Pretreatment of bovine endothelial cells with BCNU did not potentiate lysis by distilled water, calcium ionophore, lipopolysaccharide, or hypochlorous acid. Depletion of cellular reduced glutathione by reaction with DEM or CDNB or by inhibition of Glutathione synthesis by BSO also potentiated endothelial lysis by enzymatically generated hydrogen peroxide. Inhibition of endothelial Glutathione reductase by BCNU or depletion of reduced glutathione by BSO increased endothelial susceptibility to lysis by hydrogen peroxide generated by phorbol myristate acetate-activated neutrophils.
We conclude that the Glutathione redox cycle plays an important role as an endogenous Antioxidants defense mechanism in cultured endothelial cells
M Harlan, J D Levine, K S Callahan, B R Schwartz, and L A Harker
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Role of glutathione redox status in liver injury
GSH is the most abundant redox molecule in cells and thus the most important determinant of cellular redox status.
Thiols in proteins can undergo a wide range of reversible redox modifications (e.g. S-glutathionylation, S-nitrosylation, disulfide formation) during times of increased exposure to reactive oxygen and nitrogen species, which can affect protein activity.
These reversible thiol modifications regulated by GSH may be nano-switches to turn on and off proteins, similar to phosphorylation, in cells. In the cytoplasm, altered redox state can activate (e.g. MAP kinases, Nrf-2) and inhibit (e.g. phosphatases, caspases) proteins, whereas in the nucleus redox alterations can inhibit DNA binding of transcription factors (NF-kappaB, AP-1).
The consequences include promotion of expression of Antioxidants genes, and alterations of hepatocyte survival as well as the balance between necrotic versus apoptotic cell death.
Therefore the understanding of the redox regulation of proteins may have important clinical ramifications in understanding pathogenesis of liver diseases.
Han D , Hanawa N , Saberi B , Kaplowitz N
Thiols in proteins can undergo a wide range of reversible redox modifications (e.g. S-glutathionylation, S-nitrosylation, disulfide formation) during times of increased exposure to reactive oxygen and nitrogen species, which can affect protein activity.
These reversible thiol modifications regulated by GSH may be nano-switches to turn on and off proteins, similar to phosphorylation, in cells. In the cytoplasm, altered redox state can activate (e.g. MAP kinases, Nrf-2) and inhibit (e.g. phosphatases, caspases) proteins, whereas in the nucleus redox alterations can inhibit DNA binding of transcription factors (NF-kappaB, AP-1).
The consequences include promotion of expression of Antioxidants genes, and alterations of hepatocyte survival as well as the balance between necrotic versus apoptotic cell death.
Therefore the understanding of the redox regulation of proteins may have important clinical ramifications in understanding pathogenesis of liver diseases.
Han D , Hanawa N , Saberi B , Kaplowitz N
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Glutathione, stress responses, and redox signaling in lung inflammation
Changes in the ratio of intracellular reduced and disulfide forms ofGlutathione (GSH/GSSG) can affect signaling pathways that participate in various physiological responses from cell proliferation to gene expression and apoptosis.
It is also now known that many proteins have a highly conserved cysteine (sulfhydryl) sequence in their active/regulatory sites, which are primary targets of oxidative modifications and thus important components of redox signaling.
However, the mechanism by which oxidants and GSH/protein-cysteine-thiols actually participate in redox signaling still remains to be elucidated.
Initial studies involving the role of cysteine in various proteins have revealed that cysteine-SH may mediate redox signaling via reversible or irreversible oxidative modification to Cys-sulfenate or Cys-sulfinate and Cys-sulfonate species, respectively.
Oxidative stress possibly via the modification of cysteine residues activates multiple stress kinase pathways and transcription factors nuclear factor-kappaB and activator protein-1, which differentially regulate the genes for proinflammatory cytokines as well as the protective antioxidant genes. Understanding the redox signaling mechanisms for differential gene regulation may allow for the development of novel pharmacological approaches that preferentially up-regulate key antioxidant genes, which, in turn, reduce or resolve inflammation and injury.
This forum article features the current knowledge on the role of GSH in redox signaling, particularly the regulation of transcription factors and downstream signaling in lung inflammation. Rahman I , Biswas SK , Jimenez LA , Torres M , Forman HJ
Glutathione's three major roles in the body are summarized by the letters A-B-C.- Anti-oxidant- Blood Booster- Cell Detoxifier
It is also now known that many proteins have a highly conserved cysteine (sulfhydryl) sequence in their active/regulatory sites, which are primary targets of oxidative modifications and thus important components of redox signaling.
However, the mechanism by which oxidants and GSH/protein-cysteine-thiols actually participate in redox signaling still remains to be elucidated.
Initial studies involving the role of cysteine in various proteins have revealed that cysteine-SH may mediate redox signaling via reversible or irreversible oxidative modification to Cys-sulfenate or Cys-sulfinate and Cys-sulfonate species, respectively.
Oxidative stress possibly via the modification of cysteine residues activates multiple stress kinase pathways and transcription factors nuclear factor-kappaB and activator protein-1, which differentially regulate the genes for proinflammatory cytokines as well as the protective antioxidant genes. Understanding the redox signaling mechanisms for differential gene regulation may allow for the development of novel pharmacological approaches that preferentially up-regulate key antioxidant genes, which, in turn, reduce or resolve inflammation and injury.
This forum article features the current knowledge on the role of GSH in redox signaling, particularly the regulation of transcription factors and downstream signaling in lung inflammation. Rahman I , Biswas SK , Jimenez LA , Torres M , Forman HJ
Glutathione's three major roles in the body are summarized by the letters A-B-C.- Anti-oxidant- Blood Booster- Cell Detoxifier
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Wednesday, January 16, 2008
Substances that Boost Glutathione Levels and Protect Brain Cells
Taking Glutathione itself as a supplement does not boost cellular Glutathione levels, since it breaks down in the digestive tract before it reaches the cells.
However, intravenous Glutathione therapy and Glutathione precursors or dietary supplements are effective in boosting intracellular levels ofGlutathione.
Intravenous Glutathione Injections:
Intravenous Glutathione injections have been shown to produce amazing and rapid results, in patients with Parkinson's disease. Followingeven a single dosage of intravenous Glutathione, many of the symptoms of Parkinson's disease rapidly improve, often in as little as 15 minutes.
Glutathione Precursors:
In the Alzheimer's study conducted by Welsh GP, Andrew McCaddon, adding theGlutathione precursor, N-acetyl-cysteine (NAC) to a protocol thatlowered homocysteine levels by simple supplementation with B12 and folate, resulted in prompt, striking, and sustained clinical improvement in nearly all the patients.
Cucurmin (turmeric):
Studies have shown that the Indian curry spice, cucurmin, has neuroprotective effects because of its ability to induce the enzyme, hemeoxygenase-1(HO-1), which protects neurons exposed to oxidant stress. Treatment of brain cells called astrocytes, with curcumin, increases expression of HO-1 protein as well as Glutathione S-transferase.
Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7919-24. Epub 2003 Jun 05.
Am J Geriatr Psychiatry. 2003 Mar-Apr;11(2):246-9
Can Curry Protect Against Alzheimer's?; American Physiological Society (APS) Press Release; 16-Apr-2004
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
THE MAX GXL is a PATENTED High Performance Formula which:
Dramatically Raises Your Energy Level
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However, intravenous Glutathione therapy and Glutathione precursors or dietary supplements are effective in boosting intracellular levels ofGlutathione.
Intravenous Glutathione Injections:
Intravenous Glutathione injections have been shown to produce amazing and rapid results, in patients with Parkinson's disease. Followingeven a single dosage of intravenous Glutathione, many of the symptoms of Parkinson's disease rapidly improve, often in as little as 15 minutes.
Glutathione Precursors:
In the Alzheimer's study conducted by Welsh GP, Andrew McCaddon, adding theGlutathione precursor, N-acetyl-cysteine (NAC) to a protocol thatlowered homocysteine levels by simple supplementation with B12 and folate, resulted in prompt, striking, and sustained clinical improvement in nearly all the patients.
Cucurmin (turmeric):
Studies have shown that the Indian curry spice, cucurmin, has neuroprotective effects because of its ability to induce the enzyme, hemeoxygenase-1(HO-1), which protects neurons exposed to oxidant stress. Treatment of brain cells called astrocytes, with curcumin, increases expression of HO-1 protein as well as Glutathione S-transferase.
Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7919-24. Epub 2003 Jun 05.
Am J Geriatr Psychiatry. 2003 Mar-Apr;11(2):246-9
Can Curry Protect Against Alzheimer's?; American Physiological Society (APS) Press Release; 16-Apr-2004
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
THE MAX GXL is a PATENTED High Performance Formula which:
Dramatically Raises Your Energy Level
Slows Down The Aging Process
Strengthens Your Immune System
Fights Inflammation and Diseases of Aging
Improves Athletic Performance & Recovery
Detoxifies Your Body
Glutathione and Mood Disorders
Studies have found that the mood stabilizing drug, valproate, used to treat epilepsy and bi-polar disorder, regulates expression of the genes that make Glutathione-S-transferase (GST).
In addition, chronic treatment with lithium, another commonly prescribed mood stabilizer used in treating manic-depression, also increased levels of GST.
These findings led researchers to conclude that Glutathione S-transferase may be a novel target for mood stabilizing drugs.
Journal of Neurochemistry, Vol. 88, No. 6, 2004 1477-1484
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
In addition, chronic treatment with lithium, another commonly prescribed mood stabilizer used in treating manic-depression, also increased levels of GST.
These findings led researchers to conclude that Glutathione S-transferase may be a novel target for mood stabilizing drugs.
Journal of Neurochemistry, Vol. 88, No. 6, 2004 1477-1484
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
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Alzheimer's Disease and Glutathione
Free radicals and oxidative damage in neurons is known to be a primary cause of degenerative diseases like Alzheimer's disease.'
Amyloid-Я peptide (AЯ) accumulation in senile plaques, a pathological hallmark of Alzheimer's disease (AD), has been implicated in neuronal degeneration.
Amyloid plaques encroaching on the brain increase the production of free radicals, or oxidative stress. Antioxidants, such as vitamin C and E "mop up" the damaging free radicals.
Glutathione (GSH ) precursors can prevent death of brain cells induced by amyloid plaques in Alzheimer's disease, while substances that deplete GSH increase cell death.
Evidence has been piling up over the link between the amount of an amino acid called homocysteine in the blood and the chance of developing Alzheimer's.
For people not genetically predisposed to developing Alzheimer's, cholesterol and homocysteine, largely caused by an unhealthy lifestyle, are the core causal factors.
Welsh GP, Andrew McCaddon, showed that the more homocysteine that patients with Alzheimer's had, the worse their mental performance, and the worse their "cognitive impairment," the less they had of the antioxidant Glutathione.
The Journal of Cell Biology, Volume 164, Number 1, 123-131; 5 January 2004
Biol Psychiatry. 2003 Feb;53(3):254-60
Click here for more about Glutathione and its benefits to our body.
Amyloid-Я peptide (AЯ) accumulation in senile plaques, a pathological hallmark of Alzheimer's disease (AD), has been implicated in neuronal degeneration.
Amyloid plaques encroaching on the brain increase the production of free radicals, or oxidative stress. Antioxidants, such as vitamin C and E "mop up" the damaging free radicals.
Glutathione (GSH ) precursors can prevent death of brain cells induced by amyloid plaques in Alzheimer's disease, while substances that deplete GSH increase cell death.
Evidence has been piling up over the link between the amount of an amino acid called homocysteine in the blood and the chance of developing Alzheimer's.
For people not genetically predisposed to developing Alzheimer's, cholesterol and homocysteine, largely caused by an unhealthy lifestyle, are the core causal factors.
Welsh GP, Andrew McCaddon, showed that the more homocysteine that patients with Alzheimer's had, the worse their mental performance, and the worse their "cognitive impairment," the less they had of the antioxidant Glutathione.
The Journal of Cell Biology, Volume 164, Number 1, 123-131; 5 January 2004
Biol Psychiatry. 2003 Feb;53(3):254-60
Click here for more about Glutathione and its benefits to our body.
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