Modulation of oxidative stress-induced changes in hypertension and atherosclerosis by antioxidants.

Abstract

An imbalance between reactive oxygen species and antioxidant reserve, referred to as oxidative stress, results in the altered structure and function of proteins, lipids and DNA. Oxidative stress is associated with hypertension and atherosclerosis, but it is unknown whether it is a causative or resultant factor. The authors suggest that insulin resistance is the key element in the pathogenesis of these diseases, and leads to abnormal glucose and lipid metabolism with an increase in reactive aldehydes. These aldehydes react with the sulfhydryl and amino groups of proteins to form advanced glycation end products, adversely affecting body proteins, including antioxidant enzymes. This leads to oxidative stress. Advanced glycation end products and reactive oxygen species perpetuate a pro-oxidant state, producing the changes that are characteristic of hypertension and atherosclerosis. Antioxidants have been shown to modulate these changes. An ideal therapy for these diseases includes antioxidants, which attenuate insulin resistance, the source of oxidative stress.