Mercuric chloride induced reproductive toxicity associated with oxidative damage in male Wistar albino rat, Rattus norvegicus.

Abstract

In the field of toxicology, male reproductive hazards attributed to metal exposure is a fast-developing issue. Mercury has been identified as an environmental pollutant that causes potential adverse impacts on organisms. This study aimed to assess the reprotoxic consequences of mercuric chloride (HgCl₂). Five groups of sexually mature albino rats were given oral mercuric chloride (HgCl₂) treatment. (G1) control group received saline treatment; (G2) (5.25 mg/kg of HgCl₂ for 30 days); (G3) (5.25 mg/kg of HgCl₂ for 60 days); (G4) (10.5 mg/kg of HgCl₂ for 30 days); (G5) (10.5 mg/kg of HgCl₂ for 60 days). The hormonal levels, sperm count, sperm motility, sperm viability, and reproductive organ weight, including body weight, were substantially reduced, whereas the sperm abnormality rate was enhanced in rat groups treated with HgCl₂. The analysis revealed that the effect size (Cohen's d) for sperm parameters, including sperm count, motility and viability, were extremely high across all groups, except for sperm abnormality in group 2 (d = 0.59) and group 3 (d = 0.18), where moderate and small effect sizes were observed respectively, and this suggests a significant impact of the intervention on sperm parameters. The administration of HgCl₂ resulted in the induction of oxidative stress in testis that is manifested by substantially enhanced lipid peroxidation (MDA) with a substantial decrease in activity of antioxidant enzymes like catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), and glutathione peroxidase (GPx) in testes of mercury-treated groups. Concomitantly, there was downregulation in the mRNA levels of the genes involved in spermatogenesis, namely Hsp-70, insulin-like growth factor (IGF), glutathione-S-transferase, and p53 in the testis. The expression of antiapoptotic protein B cell lymphoma (Bcl-2) was decreased, and conversely, the expression of cell proliferative protein Ki-67 was increased in a dose- and duration-dependent manner. Histopathological studies showed degenerative changes in the testis, epididymis, prostate gland, and seminal vesicle, compared to the control group. All the evidence suggests that after mercury exposure, there may be an imbalance between the body's defenses against free radicals and antioxidants, making the testis more susceptible to oxidative damage. This imbalance could potentially have a detrimental effect on the function of the male reproductive system.