Oxidative Stress as a Mediator of Cardiovascular Disease

Abstract

During physiological processes molecules undergo chemical changes involving reducing and oxidizing reactions. A molecule with an unpaired electron can combine with a molecule capable of donating an electron. The donation of an electron is termed as oxidation whereas the gaining of an electron is called reduction. Reduction and oxidation can render the reduced molecule unstable and make it free to react with other molecules to cause damage to cellular and sub-cellular components such as membranes, proteins and DNA. In this paper, we have discussed the formation of reactive oxidant species originating from a variety of sources such as nitric oxide (NO) synthase (NOS), xanthine oxidases (XO), the cyclooxygenases, nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase isoforms and metal-catalyzed reactions. In addition, we present a treatise on the physiological defences such as specialized enzymes and antioxidants that maintain reduction-oxidation (redox) balance. We have also given an account of how enzymes and antioxidants can be exhausted by the excessive production of reactive oxidant species (ROS) resulting in oxidative stress/nitrosative stress, a process that is an important mediator of cell damage. Important aspects of redox imbalance that triggers the activity of a number of signaling pathways including transcription factors activity, a process that is ubiquitous in cardiovascular disease related to ischemia/reperfusion injury have also been presented.

Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

“…As we have observed in our previous studies (19), a return of the increase in the tissue MDA level in the I/R group, and a decrease in the GSH levels back to normal with quercetin treatment, is a result of the antioxidant effect of quercetin. It is well known that ischemia, together with oxidative stress and reactive oxygen products, arise as a result of oxidative stress (2). ROS activates NF-κB, which is a transcription factor responsible for the production of adhesion molecules and cytokines.…”

“…Ischemia is associated with oxidative stress and apoptosis. Oxidative stress is known to be a result of the imbalance between the production of reactive oxygen species (ROS), antioxidants and repair processes (2). Lipid peroxidation, mediated by ROS, is believed to be an important cause of destruction and damage to cell membranes during oxidative stress (3).…”

Postprandial antioxidant gene expression is modified by Mediterranean diet supplemented with coenzyme Q10 in elderly men and women

“…Although the fundamental mechanisms are still poorly understood, a growing body of evidence points toward the oxidative damage caused by reactive oxygen species (ROS) as one of the primary determinant of aging (Droge 2002). A certain amount of oxidative damage takes place even under normal conditions; however, the rate of this damage increases during the pathological conditions like diabetes, cardiovascular diseases, cancer, and aging-related diseases (Elahi et al 2009). Although aging is an inevitable event, linked to the pass of time, nutritional intervention may influence the intrinsic rate of aging as well as the incidence of these age-associated diseases.…”

The Role of Biomarkers of Oxidative Stress in Breast Cancer Risk and Prognosis: A Systematic Review of the Epidemiologic Literature

“…[1][2][3][4] Oxidative stress can be broadly defined as an imbalance between oxidants and antioxidants in favor of the oxidants, potentially leading to damage. 5,6 If the level of reactive species is high and overcomes the antioxidant defense mechanisms of the human body, oxidative damage can occur to lipids, proteins, or directly to DNA.…”