Abstract

Oxidative stress has been considered universally and undeniably implicated in the pathogenesis of all major diseases, including those of the cardiovascular system. Oxidative stress activate transcriptional messengers, such as nuclear factor—κB, tangibly contributing to endothelial dysfunction, the initiation and progression of atherosclerosis, irreversible damage after ischemic reperfusion, and even arrhythmia, such as atrial fibrillation. Evidence is rapidly accumulating to support the role of reactive oxygen species (ROS) and reactive nitrogen species (RNS) as intracellular signaling molecules. Despite this connection between oxidative stress and cardiovascular disease (CVD), there are currently no recognized therapeutic interventions to address this important unmet need. Antioxidants that provide a broad, “upstream” approach via ROS/RNS quenching or free radical chain breaking seem an appropriate therapeutic option based on epidemiologic, dietary, and in vivo animal model data. Short-term dietary intervention trials suggest that diets rich in fruit and vegetable intake lead to improvements in coronary risk factors and reduce cardiovascular mortality. Carotenoids are such abundant, plant-derived, fat-soluble pigments that functions as antioxidants. They are stored in the liver or adipose tissue, and are lipid soluble by becoming incorporated into plasma lipoprotein particles during transport. For these reasons, carotenoids may represent one plausible mechanism by which fruits and vegetables reduce the risk of chronic diseases as cardiovascular disease (CVD). This review paper outlines the role of carotenoids in maintaining cardiac health and cardioprotection mediated by several mechanisms including redox signaling.

Highlights

  • Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play important roles in regulation of cell survival

  • Nature has endowed each cell with adequate protective mechanisms against any harmful effects of free radicals: superoxide dismutase (SOD), glutathione peroxidase, glutathione reductase, thioredoxin, thiols and disulfide bonding are buffering systems in every cell. α-Tocopherol is an essential nutrient which functions as a chain-breaking antioxidant which prevents the propagation of free radical reactions in all cell membranes in the human body

  • The results indicated that the distinct effects of carotenoids on lipid peroxidation are due to membrane structure changes [46]

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Summary

Introduction

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play important roles in regulation of cell survival. When the redox homeostasis is disturbed, oxidative stress may lead to aberrant cell death and contribute to disease development [1]. Oxidative stress describes various deleterious processes resulting from an imbalance between the excessive formation of reactive oxygen and/or nitrogen species and limited antioxidant defenses [2]. In this regard, cardiovascular risk factors significantly cause oxidative stress, which contributes to a disruption in the balance between nitric oxide (NO) and reactive oxygen species, with a resulting relative decrease in NO bioavailability. In the post-ischemic myocardium, elevated levels of exogenous ROS are generated in cardiomyocytes, endothelial cells, and infiltrating neutrophils that can lead to cellular dysfunction and necrosis. The present review outlines the role of various carotenoids in cardiac health and cardioprotection mediated by several mechanisms including redox signaling

Mechanisms of Redox Signaling
Antioxidants in Redox Status
Carotenoids as Redox Agents
Structure of Carotenoids
Bioavailability and Metabolism of Carotenoids
Antioxidant Activity
Hypocholesterolemic Activity
Antiinflammatory Activity
Role on Endothelial Function
Influence on Gap Junction Communication
Attenuation of Ischemia-Reperfusion Injury
Conclusions
Methods
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