Molecular Basis for Mercury-Induced Alteration in Endothelial Function: NO and its Modulators

Omanwar S,Saidullah B

doi:10.4172/2329-6607.1000167

Abstract

Epidemiological and animal studies have suggested a strong association between the environmental and occupational exposure to mercury and risk of cardiovascular diseases (CVD). One of the triggering factors of CVD is endothelial dysfunction. The endothelium can evoke relaxations and contractions of the underlying smooth muscle, by releasing vasoactive agents. Nitric oxide (NO), formed by endothelial NO synthase (eNOS), is the best characterized endothelium derived relaxing factor (EDRF). The release of NO is down regulated/upregulated by factors like oxidative stress, estrogen and diseases like diabetes and hypercholelestrolemia, etc. The inhibition/ activation of eNOS by mercury, affecting the NO release is one of the proposed mechanisms for mercury-induced vascular diseases. In addition, during exposure to mercury, overproduction of reactive oxygen species (ROS) can occur, resulting in oxidative stress, which is another major risk factor for endothelial dysfunction. In this article, molecular basis for mercury-mediated alteration in endothelium derived vasodilator (NO) and factors modulating the release of NO are being reviewed.

Highlights

For many years, the vascular endothelium, a monolayer of cells covering the vascular lumen was thought to be relatively inert
Vascular endothelial cells respond to low concentration of mercury by releasing Nitric oxide (NO), which relaxes the vascular smooth muscle that surrounds them
Decrease/increase in release of NO on mercury exposure is majorly regulated by superoxide anions and minorly may be by insulin, estrogen, omega-3 unsaturated fatty acid and hypercholesterolemia