Protective effect of selenium against aluminium chloride induced cardiotoxicity in rats

Aluminium (Al) is broadly dispersed throughout the natural and industrial environment (1). It is widely used in daily life causing its easy exposure to animals and human beings. Al sources are mainly corn, yellow cheese, salt, herbs, spices, tea, cosmetics, ware, and containers. It has been reported that Al could accumulate in all tissues of animals, preferentially in liver, heart, bones and brain (2). This metal disrupts the prooxidant/antioxidant balance in tissues leading to biochemical and physiological dysfunction due to an excessive reactive oxygen species (ROS) generation (3,4). Chronic aluminium exposure results in a decreased activity of complexes I, II and IV of electron transport chain leading to the impairment of mitochondrial energy metabolism and oxidative damage (5). Oxidative stress may play a crucial role in cardiac and vascular abnormalities in different types of cardiovascular diseases (6). The mechanism by which Al produces cardiotoxicity effects may be attributed to oxidative stress and disturbance of the intracellular redox system.Supplementation of antioxidants can be considered as an alternative method to alleviate metals induced oxidative heart damage. Selenium (Se) is generally recognized to be a trace element of great importance for human health which protects the cells from the harmful effects of free radicals attack (7). Previous studies have confirmed the protective effects of Se against free-radical induced cardiac injury (8,9). It plays an important role in many physiological processes including the biosynthesis of coenzyme Q, regulation of ion fluxes across membranes and stimulation of immune function (10). The beneficial effect of Se is attributed to selenoproteins such as glutathione peroxidase and thioredoxin reductase. The underlying mechanisms of Al-induced toxicity are not entirely clear; however, they are apparently related to its pro-oxidant effects. To our knowledge, findings concerning the cardiotoxic effects of Al remain scarce and appear to be lacking. In an effort to better our understanding on aluminum heart toxicity mechanism, the present study was designed to explore whether the administration of this metal induced heart tissue damage in adult rats and to evaluate the possible ameliorative effect of Se.