Chapter 30 - Molecular mechanisms of oxidative stress in aging: Free radicals, aging, antioxidants and disease

Abstract

This chapter discusses the molecular mechanisms of oxidative stress in aging. Aging has a strong genetic component, but it can be viewed partly as a degenerative process dictated by free radical reactions, possibly increasing the incidence of several degenerative disease states. Free radicals increase with age, alter physiological functions, increase disease states, and accelerate pathophysiological conditions. Major discoveries substantiating the free radical theory of aging in free radical biology have been made in the past few decades. Many scientific papers and a multitude of scientific disciplines have established a strong relationship between free radical biology and pathophysiology. The chapter discusses several major sources of free radical oxidant production in vivo and their relationship to aging and several degenerative diseases of aging. The mitochondria and phagocytes are potent sources of oxidant formation and may cause damage to DNA, lipids, and proteins generating unnatural structures. The altered biomolecules may play a critical role in the development of degenerative diseases and the aging process itself. Specific protein modifications can alter enzyme function or cell-signaling ability; certain altered biomolecules that accumulate can affect protein function. Scientific evidence has shown that several interventions—such as dietary restriction, chronic exercise, and antioxidant therapies—can attenuate the aging process and disease states. Therapies have been developed to reduce oxidative stress and protect against the development of degenerative diseases, such as atherosclerosis, Alzheimer's disease, and Parkinson's disease.