Research Output Details

Reactive oxygen species in health and disease

Published 75
Authors:

Alfadda; Sallam

Journal/Publication:

Journal of Biomedicine and Biotechnology

Publication Date:

Jan-2012

Keywords:

alpha tocopherol antioxidant curcumin diclofenac dithiothreitol doxycycline ginsenoside Rb 1 mangiferin placebo polyphenol derivative reactive oxygen metabolite recombinant erythropoietin resveratrol rottlerin tert butyl hydroperoxide antiinflammatory activity antioxidant activity blood vessel diameter cell metabolism chronic inflammation comorbidity diabetes mellitus diseases drug mechanism endoplasmic reticulum endoplasmic reticulum stress genomic instability health human immune system infection insulin resistance metabolic disorder mitochondrion neoplasm nonhuman obesity oxidation reduction reaction oxidative stress oxygen sensing pathogenesis regulatory mechanism review signal transduction skeletal muscle toxicity transcription regulation animal drug effect metabolism Animals Antioxidants Disease Health Humans Oxidation-Reduction Oxidative Stress Reactive Oxygen Species

Abstract

During the past decades, it became obvious that reactive oxygen species (ROS) exert a multitude of biological effects covering a wide spectrum that ranges from physiological regulatory functions to damaging alterations participating in the pathogenesis of increasing number of diseases. This review summarizes the key roles played by the ROS in both health and disease. ROS are metabolic products arising from various cells; two cellular organelles are intimately involved in their production and metabolism, namely, the endoplasmic reticulum and the mitochondria. Updates on research that tremendously aided in confirming the fundamental roles of both organelles in redox regulation will be discussed as well. Although not comprehensive, this review will provide brief perspective on some of the current research conducted in this area for better understanding of the ROS actions in various conditions of health and disease. © 2012 Assim A. Alfadda and Reem M. Sallam.