Sources and Effects of Oxidants

Four endogenous sources appear to account for most of the oxidants produced by cells:

1) As a consequence of normal aerobic respiration, mitochondria consume molecular oxygen, reducing it by sequential steps to produce H20. Inevitable by-products of this process, as stated above, are O2.-, H202, and .OH. About l012 oxygen molecules are processed by each rat cell daily, and the leakage of partially reduced oxygen molecules is about 2%, yielding about 2x1010 superoxide and hydrogen peroxide molecules per cell per day.

2) Phagocytic cells destroy bacteria or virus-infected cells with an oxidative burst of NO, O2.-, H2O2, and [[macron]]OCl. Chronic infection by viruses, bacteria, or parasites, results in a chronic phagocytic activity and consequent chronic inflammation, which is a major risk factor for cancer. Chronic infections are particularly prevalent in third world countries.

3) Peroxisomes, which are organelles responsible for degrading fatty acids and other molecules, produce H202 as a byproduct, which is then degraded by catalase. Evidence suggests that, under certain conditions, some of the peroxide escapes degradation, resulting in its release into other compartments of the cell and in increased oxidative DNA damage.

4) Cytochrome P450 enzymes in animals constitute one of the primary defense systems against natural toxic chemicals from plants, the major source of dietary toxins. The induction of these enzymes, prevent acute toxic effects from foreign chemicals, but also results in oxidant by-products that damage DNA (Park, J.-Y. K. and Ames, B.N., unpublished).

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Three exogenous sources may significantly increase the large endogenous oxidant load.

1) The oxides of nitrogen (NOx) in cigarette smoke (about 1000 ppm) cause oxidation of macromolecules, and deplete antioxidant levels. This is likely to contribute significantly to the pathology of smoking. Smoking is a risk factor for heart disease as well as a wide variety of cancers in addition to lung cancer.

2) Iron (and copper) salts promote the generation of oxidizing radicals from peroxides (Fenton chemistry). Men who absorb significantly more than normal amounts of dietary iron due to a genetic defect (hemochromatosis disease) are at an increased risk for both cancer and heart disease. It has therefore been argued that too much dietary copper or iron, particularly heme iron (which is high in meat), is a risk factor for cardiovascular disease and cancer in normal men

3) Normal diets contain plant food with large amounts of natural phenolic compounds, such as chlorogenic and caffeic acid, that may generate oxidants by redox cycling .

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