The proliferation of T and B cells, natural killer cells, and lymphokine activated killer cells that are required to mount an effective defense against pathogens and tumor cells appear to be inhibited markedly with age and upon exposure to oxidants. These effects can, in part, be counteracted in elderly individuals by dietary antioxidant supplementation. While the endogenous sources of oxidants that lead to the suppression of lymphocyte dependent immunity are not known, in vitro studies have demonstrated that polymorphonuclear leucocytes and macrophages, both can inhibit proliferation of various lymphocyte subpopulations through the production of reactive oxygen intermediates and the prostaglandin metabolite PGE2 as well as from nitric oxide.
This suggests that conditions that involve infiltration of polymorphonuclear leucocytes and macrophages (i.e., chronic inflammatory diseases), could result in compromised lymphocyte function. The suppressive effects of macrophages on mitogen induced lymphocyte proliferation can be reversed partially by thiol reagents, catalase or indomethacin, or by NG-monomethyl-L-arginine, a competitive inhibitor of nitric oxide synthesis.
The age associated decrease in cell mediated immunity may be due to a decreased level of certain small molecule antioxidant and antioxidant enzymes that accompany the aging process.
Calorie restriction, a dietary regimen that increases maximal lifespan in rodents also enhances T lymphocyte responsiveness possibly by slowing the rate of thymus involution and by boosting the level of cellular antioxidant defenses.
Showing posts with label age-related. Show all posts
Showing posts with label age-related. Show all posts
Monday, February 11, 2008
Aging is slowed by calorie or protein restriction
In rodents a calorie restricted diet, significantly increases lifespan, decreases reproduction, and markedly decreases cancer rates.
It has been suggested that Darwinian fitness in animals is increased by the delay of reproductive function during periods of low food availability and that the saved resources are invested in maintenance of the body until food resources are available for successful reproduction.
Protein restriction appears to have the same effects on rodents as calorie restriction, though it is less well-studied. An understanding of mechanisms for this marked effect on aging and cancer is becoming clearer and may in good part be due to reduced oxidative damage.
The suggestion that maintenance functions are enhanced in calorie-restricted rats thus resulting in less oxidative damage is supported by the findings of more efficient DNA repair, better coupled mitochondrial respiration and a delay in the age-dependent decline of antioxidant defenses.
The higher level of antioxidant defenses could also account for the enhanced immune response in restricted animals. We have recently shown that either calorie or protein restriction decreases the rate of accumulation of oxidized protein that accompanies aging in rats and preliminary results suggest a decrease in preneoplastic foci and oxidative lesions in DNA as well.
Thus, the overall effect of these enhanced maintenance activities appears to be a reduction in oxidative damage to DNA and protein, a decrease in DNA and protein lesions, and a decrease in somatic mutations. Markedly lower mitotic rates are observed in a variety of tissues in calorie restricted compared to ad libitum fed rodent, which may also contribute to the decrease in tumor incidence.
Click here for more about Glutathione and its benefits to our body.
*Dietary restriction activates the pituitary adrenocorticotropic axis resulting in a decrease in the release of reproductive and mitogenic hormones. Decreases in mitogenic hormones such as insulin, TSH, growth hormone, estrogen, and prolactin decrease the likelihood of hormone-induced cancers, as has been shown in various animal studies. This is consistent with suppression of mitogenic hormones and decreased proto-oncogene expression. The lowered incidence of mammary tumors observed in calorie-restricted rats has been attributed to reduced circulating levels of the mammotropic hormones estrogen and prolactin.
Click here for more about Glutathione and its benefits to our body.
It has been suggested that Darwinian fitness in animals is increased by the delay of reproductive function during periods of low food availability and that the saved resources are invested in maintenance of the body until food resources are available for successful reproduction.
Protein restriction appears to have the same effects on rodents as calorie restriction, though it is less well-studied. An understanding of mechanisms for this marked effect on aging and cancer is becoming clearer and may in good part be due to reduced oxidative damage.
The suggestion that maintenance functions are enhanced in calorie-restricted rats thus resulting in less oxidative damage is supported by the findings of more efficient DNA repair, better coupled mitochondrial respiration and a delay in the age-dependent decline of antioxidant defenses.
The higher level of antioxidant defenses could also account for the enhanced immune response in restricted animals. We have recently shown that either calorie or protein restriction decreases the rate of accumulation of oxidized protein that accompanies aging in rats and preliminary results suggest a decrease in preneoplastic foci and oxidative lesions in DNA as well.
Thus, the overall effect of these enhanced maintenance activities appears to be a reduction in oxidative damage to DNA and protein, a decrease in DNA and protein lesions, and a decrease in somatic mutations. Markedly lower mitotic rates are observed in a variety of tissues in calorie restricted compared to ad libitum fed rodent, which may also contribute to the decrease in tumor incidence.
Click here for more about Glutathione and its benefits to our body.
*Dietary restriction activates the pituitary adrenocorticotropic axis resulting in a decrease in the release of reproductive and mitogenic hormones. Decreases in mitogenic hormones such as insulin, TSH, growth hormone, estrogen, and prolactin decrease the likelihood of hormone-induced cancers, as has been shown in various animal studies. This is consistent with suppression of mitogenic hormones and decreased proto-oncogene expression. The lowered incidence of mammary tumors observed in calorie-restricted rats has been attributed to reduced circulating levels of the mammotropic hormones estrogen and prolactin.
Click here for more about Glutathione and its benefits to our body.
Aging and Dietary Restriction
Evolutionary biologists have argued that aging is inevitable because of several tradeoffs. One tradeoff is that a considerable proportion of an animal's resources is devoted to reproduction at a cost to maintenance, which means that the maintenance of somatic tissues is less than that required for indefinite survival. Of the vast array of maintenance processes that are necessary to sustain normal function in somatic cells, those that defend the cell against metabolism derived oxidants are likely to play an important role.
Metabolism has costs: oxidants by-products of normal energy metabolism extensively damage DNA, proteins, and other molecules in the cell, and this damage accumulates with age.
Another tradeoff is that nature selects for many genes that have immediate survival value, but that may have long term deleterious consequences. The oxidative burst from phagocytic cells, for example, protects against death from bacterial and viral infections, but contributes to DNA damage, mutation, and cancer.
Click here for more about Glutathione and its benefits to our body.
Metabolism has costs: oxidants by-products of normal energy metabolism extensively damage DNA, proteins, and other molecules in the cell, and this damage accumulates with age.
Another tradeoff is that nature selects for many genes that have immediate survival value, but that may have long term deleterious consequences. The oxidative burst from phagocytic cells, for example, protects against death from bacterial and viral infections, but contributes to DNA damage, mutation, and cancer.
Click here for more about Glutathione and its benefits to our body.
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.
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