The idea that oxidative stress may play an important role in many chronic diseases and, indeed, in the aging process itself is not a new one. 1,2 Cancer, heart disease, and cataracts are but a few of the diseases for which an oxidative mechanism has been invoked. 3 Despite wide‐spread speculation, our understanding of the role of oxidative stress in aging and disease causation is still fragmentary and incomplete. Oxidation of glucose and fats is central to energy generation in all mammalian cells, and thus, in a sense, is synonymous with life itself. Some byproducts of oxidation have an unpaired electron, and these “free radicals” and closely related reactive oxygen species are highly and indiscriminately reactive with nearby molecules, damaging proteins, lipids, and nucleic acids. In addition to the oxidative damage secondary to normal cellular metabolism, other sources of oxidative stress include endogenous substances generated in response to infection and ischemia, ionizing radiation, and compounds in the environment (e.g., those in cigarette smoke). There are a number of strategies for limiting oxidative damage. 4,5 Oxidative processes within the cell tend to be compartmentalized in mitochondria and other organelles such as peroxisomes, thereby placing physical distance between oxidative processes
Journal of American Geriatrics Society – Wiley
Published: Jul 1, 1996
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