ABSTRACT
Oxidative stress is experienced because of a variance between the manufacturing of reactive species and the body’s potential to overcome them by utilizing antioxidants. Individual genetic adaptation impacts the digestion of exogenous antioxidants that are consumed from regular meals and eventually participates in the expansion of oxidative stress. While alteration in the quality of gene coding might affect the endogenous cell reinforcement protein’s enzymatic action, and accordingly, increase the level of reactive species, oxidative stress, and the probability of disease evolution, oxidative stress has been reported to increase the progression of various diseases like type-2 diabetes, cardiovascular disorders, malignant tumors, Alzheimer’s disease, and rheumatoid arthritis. Maximum oxidative stress can create impaired functional homeostasis, depicting human aging. Aging seems to have an advanced conservative stress response framework, presumably obtained from an amalgam of a diet containing natural antioxidants, 46a dynamic lifestyle, and a positive genetic establishment, particularly rich in hereditary variations ready to neutralize the stress burden. The blend of these variables could permit aging to keep up with moderate degrees of free radicals that produce profitable signaling and modulator effects on cellular metabolism. Herein, we attempt to focus on the current knowledge of genetic variance in human genes related to oxidative stress. Highlighting the study of genetic variation will be a useful approach for determining the impact of oxidative stress in diversified diseases and human aging.
