Title: Antioxidant adaptation: a unified disease theory
Abstract: Free radical-mediated oxidative stress to cells and tissues can generate activated oxygen species and lipid peroxides, which mediate inflammatory/immune symptomatologies and are associated with degenerative disease states and possibly with environmental illness (Levine and Reinhardt, 1983. J. Orthomol. Psychiatry 12,166-183). Rats and mice experimentally exposed to high doses of chemical oxidant stressors can become tolerant as a consequence of antioxidant adaptation. Tolerance is characterized by increased activity of glutathione peroxidase (GP), a key antioxidant enzyme which detoxifies peroxide species, subject to adequate availability of its metal cofactor (selenium) and its cosubstrate (reduced glutathione). Increases in other enzymes of the glutathione pathway (glutathione reductase and glucose-6-phosphate dehydrogenase, among others) also are essential. Humans also may adapt biochemically to oxidative stress. In those inherited disease states characterized by abnormally elevated endogenous oxidative stress, peroxide production is enhanced in selected tissues and GP activity is correspondingly increased. GP activity is also abnormally altered (increased or decreased) in other disease states characterized by increased tissue lipid peroxide levels. The price of continued adaptation for humans, as for laboratory animals, may be premature progression to degenerative disease. Herein we hypothesize a four-stage clinical progression to degenerative disease, in individuals subject to sustained oxidative stress. This trend may be interrupted or reversed by the cessation of oxidative stress and dietary replenishment of essential antioxidant factors. We suggest that glutathione peroxidase activity (along with other biochemical indicators of oxidative stress) appears to be a valuable marker enzyme for monitoring the clinical response to nutritional antioxidant therapy. In this article we review the evidence that laboratory animals and humans can adapt to acute oxidative stress, by augmenting . Director of Research Allergy Research Group 400 Preda St. San Leandro, CA 94577 . Director, Biocurrents Division, Allergy Research Group
Publication Year: 1985
Publication Date: 1985-01-01
Language: en
Type: article
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Cited By Count: 4
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