» Articles » PMID: 39738833

Mercuric Chloride Induced Reproductive Toxicity Associated with Oxidative Damage in Male Wistar Albino Rat, Rattus Norvegicus

Overview
Specialty Pharmacology
Date 2024 Dec 31
PMID 39738833
Authors
Affiliations
Soon will be listed here.
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 (HgCl). Five groups of sexually mature albino rats were given oral mercuric chloride (HgCl) treatment. (G1) control group received saline treatment; (G2) (5.25 mg/kg of HgCl for 30 days); (G3) (5.25 mg/kg of HgCl for 60 days); (G4) (10.5 mg/kg of HgCl for 30 days); (G5) (10.5 mg/kg of HgCl 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 HgCl. 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 HgCl 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.

References
1.
Acharya U, Mishra M, Patro J, Panda M . Effect of vitamins C and E on spermatogenesis in mice exposed to cadmium. Reprod Toxicol. 2007; 25(1):84-8. DOI: 10.1016/j.reprotox.2007.10.004. View

2.
Adelakun S, Ukwenya V, Akingbade G, Omotoso O, Aniah J . Interventions of aqueous extract of Solanum melongena fruits (garden eggs) on mercury chloride induced testicular toxicity in adult male Wistar rats. Biomed J. 2020; 43(2):174-182. PMC: 7283571. DOI: 10.1016/j.bj.2019.07.004. View

3.
Basu A, Haldar S . The relationship between BcI2, Bax and p53: consequences for cell cycle progression and cell death. Mol Hum Reprod. 1999; 4(12):1099-109. DOI: 10.1093/molehr/4.12.1099. View

4.
Bauche F, Fouchard M, Jegou B . Antioxidant system in rat testicular cells. FEBS Lett. 1994; 349(3):392-6. DOI: 10.1016/0014-5793(94)00709-8. View

5.
Boess F, Kamber M, Romer S, Gasser R, Muller D, Albertini S . Gene expression in two hepatic cell lines, cultured primary hepatocytes, and liver slices compared to the in vivo liver gene expression in rats: possible implications for toxicogenomics use of in vitro systems. Toxicol Sci. 2003; 73(2):386-402. DOI: 10.1093/toxsci/kfg064. View