. "2 Vitamin C, Vitamin E, Selenium, and •-Carotene and Other Carotenoids: Overview, Antioxidant Definition, and Relationship to Chronic Disease." Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, DC: The National Academies Press, 2000.
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids
antioxidants in humans is still controversial. Therefore, β-carotene does not meet the definition of a dietary antioxidant. Similar conclusions have been drawn for α-carotene, β-cryptoxanthin, lycopene, lutein, and zeaxanthin.
OXIDATIVE STRESS, ANTIOXIDANTS, AND CHRONIC DISEASE
There have been many proposals as to how oxidative stress can be defined. Because all cells are exposed to oxidants, generated either endogenously from metabolism or exogenously from a variety of environmental insults, the problem arises as to what constitutes an oxidative stress. Furthermore, different cells can be exposed to the same level of oxidants, but depending on the level of antioxidants or protective mechanisms available to the cell, they may or may not experience an oxidative stress. Sies (1985) defined oxidative stress as “a disturbance in the prooxidant-antioxidant balance in favor of the former.” Others have amplified this definition to include “short-and/or long-term disturbance of the prooxidant-antioxidant balance resulting in adverse effects that are due either to impaired antioxidation or to favored prooxidation” (Biesalski et al., 1997). Here, oxidative stress is defined as an imbalance between the production of various reactive species and the ability of the organism's natural protective mechanisms to cope with these reactive compounds and prevent adverse effects.
The primary reactive species include reactive oxygen species (ROS) and reactive nitrogen species (RNS). These in turn react in the body and generate radical intermediates of lipids, proteins, and nucleic acids that ultimately form the chemical end products of oxidative stress. The physiological consequences of these end products have been hypothesized to be the causes of many chronic diseases as well as the natural aging process (Ames, 1998; Halliwell, 1997). The protective mechanisms include protective enzymes, antioxidant or quenching compounds produced by the organism, and similar compounds made available in the diet. The evidence that chronic disease results from an imbalance between formation and removal of reactive species is discussed below.
The primary defensive compounds are antioxidants that can interact with and quench reactive radical species, and enzymes that can inactivate these species or their products. All of the compounds in this report —vitamin C, vitamin E, selenium in the form of selenoproteins, and β-carotene and other carotenoids—are in vitro