Effects of Nitric Oxide Activity on the Induction of Oxidative Stress in Skin Cell Signalling, Migration and Apoptosis


Oxidative stress is a phenomenon caused by an imbalance between production and accumulation of oxygen reactive species (ROS) in cells and tissues and the ability of a biological system to detoxify these reactive products. ROS can play, and in fact they do it, several physiological roles (i.e., cell signaling), and they are normally generated as byproducts of oxygen metabolism; despite this, environmental stressors (i.e., UV, ionizing radiations, pollutants, and heavy metals) and xenobiotics (i.e., antiblastic drugs) contribute to greatly increase ROS production, therefore causing the imbalance that leads to cell and tissue damage (oxidative stress).

Nitric oxide (NO) is a gas with a short half-life (about a few seconds) and has been reported for its diverse biochemical and physiological potentials. This molecule was first discovered in 1978 and nominated as the molecule of the year in 1992. NO is an inner cell and intra cell messenger that plays a key role in the maintenance of body hemostasis. In general, NO accomplishes its function by synthesizing cyclic guanosine monophosphate (cGMP). NO is produced from L-arginine amino acid that synthesis is mediated by nitric oxide synthases (NOS). This enzyme occurs in three major isoforms, nervous, endothelial, and induction. NO cascades result differently in various tissues, e.g., emerging as a vasodilator factor known as endothelium-derived relaxing factor (EDRF) in the cardiovascular system. However, in the nervous system, it is considered as a neurotransmitter. In addition, in some cases, it causes neutrophil-induced cell toxicity, platelet aggregation, blood flow, synaptic transmission, and long-term memory loss. Furthermore, NO is synthesized by a group of enzymes known as NOS. Three major isoforms of NOS can be detected, including nervous NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS). Recently, mitochondrial NOS has been discovered, which specifically can be found in the mitochondrion.

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Kathy Andrews
Managing Editor
Journal of Clinical & Experimental Dermatology Research