Efeito da exposição crônica ao cloreto de mercúrio (HGCL2) no sistema reprodutor de ratos machos

Abstract

Mercury is an ubiquitous environmental pollutant, its contamination and toxicity is a serious hazard to human health. Although several studies have demonstrated that mercury impairs male reproductive function at high levels, these effects and mechanisms at low levels of exposure are unknown. Therefore, the aim of this study was to investigate the effects of chronic exposure to low concentrations of HgCl2 on male reproductive system of rats. In order to study, three-month-old male Wistar rats were treated for 30 days and divided in Control (saline - i.m. - intramuscular injection) and HgCl2 group (i.m. 1st dose: 4.6 μg/kg, subsequent doses 0.07 μg/kg/day). We analyzed sperm parameters (count, motility, morphology and membrane integrity), histopathology (testis and epididymis), hormonal levels and biomarkers of oxidative stress in testis, epididymis, prostate and vas deferens. The mercury treatment caused histopathological changes in testis, loss of sperm membrane integrity, reduction in sperm quantify (testis and epididymis), reduction in daily sperm production, following by decrease in sperm motility and increase on head and tail morphologic abnormalities in spermatozoa. HgCl2 treatment increased levels of oxidative stress in reproductive organs, represented by augmented lipid peroxidation and reactive species levels as well as decreased on non-protein thiois levels (NPSH and GSH). Mercury exposure caused changes on antioxidant enzymes activity: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST) and glutathione reductase (GR) in reproductive organs. HgCl2 - chronic treatment increased GPx4 protein expression in testis of male rats and did not change luteinizing hormone (LH) levels. Ours results demonstrate, for the first time, that a 30-day chronic exposure to low doses of HgCl2 causes male reproductive toxicity and increases oxidative stress in reproductive organs of male rats which point to the oxidative stress, at least in part, as a toxicity mechanism of mercury in this system.