Can selenium supplementation modify oxidative stress in-vitro? A role for selenium supplementation in the prevention of cardiovascular disease

Abstract

Background Two thirds of the UK population are either overweight or obese (body mass index (BMI) 25-29.9 and >30 kg/m respectively) and are typically characterised by systemic oxidative stress (OS); deemed to play a key role in cardiovascular disease (CVD) development. OS results from chronically high reactive oxidative species (ROS) formation and reduced antioxidant status. OS plays a key role in CVD development by initiating atherosclerosis (fatty plaque accumulation within the arterial walls); therefore obese individuals are at increased risk of atherosclerosis development. Increased monocyte ROS generation instigates atherosclerotic plaque formation by increasing the recruitment, binding and transmigration of monocytes across arterial endothelial cells and into the arterial wall. An increased dietary antioxidant intake or up-regulation of endogenous antioxidant enzymes may counteract this OS state and therefore lower CVD risk. Selenium is an essential dietary micronutrient incorporated within the catalytic site of endogenous antioxidant Glutathione Peroxidase (GPx) enzymes, which protect cells from OS and consequent cell damage. There is, however, a lack of knowledge concerning the effect of selenium supplementation in an OS state representative of sedentary overweight/obese individuals. The aim of this work was to investigate the ability of selenium supplementation to modify monocyte cell viability/ROS production under OS. Materials and methods U937 monocyte cells were supplemented with sodium selenite (Na2SeO3; 100nM or 200nM) or not and cultured for 48 hours at 37°C. Paraquat (100mM) and S-Nitroso-Nacetyl-DL-penicillamine (10mM) (PQ/SNAP) were added to the cells to induce OS. Cell viability was assessed via MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay while ROS production was determined by Flow Cytometry using the reagent CM-H2DC-FDA.