Genetic determinants of dietary antioxidant status

Abstract

Oxidative stress refers to a physiological state in which an imbalance between pro-oxidants and antioxidants results in oxidative damage. Oxidative stress has been associated with the development of numerous chronic diseases such as type 2 diabetes, cardiovascular disease (CVD), osteoporosis, and cancer. Endogenous production of free radicals occurs during normal physiological processes, such as aerobic metabolism, oxidation of biological molecules, and enzymatic activity. Environmental factors such as ultraviolet radiation, air pollution, and cigarette smoking can also contribute to the accumulation of free radicals in the body. Excess free radicals can damage tissues and promote the upregulation of disease-related pathways such as inflammation. Modulating oxidative stress by dietary supplementation with antioxidant micronutrients such as vitamins C and E or phytochemicals such as different carotenoids may help prevent or delay the development of certain diseases. However, research on antioxidant supplementation and disease has yielded inconsistent findings, which may be due, in part, to interindividual genetic variation. Polymorphisms in genes coding for endogenous antioxidant enzymes or proteins responsible for the absorption, transport, distribution, or metabolism of dietary antioxidants have been shown to affect antioxidant status and response to supplementation. These genetic variants may also interact with environmental factors, such as diet, to determine an individual's overall antioxidant status. This chapter examines current knowledge of the relationship between genetic variation and dietary antioxidant status.