Sampada M P, David Muniswamy
Zoology, Karnataka University, Dharwad, Karnataka, 580003, India.
Naunyn Schmiedebergs Arch Pharmacol. 2024 Dec 30. doi: 10.1007/s00210-024-03585-8.
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.
在毒理学领域,金属暴露对男性生殖系统的危害是一个快速发展的研究课题。汞已被确认为一种环境污染物,会对生物体造成潜在的不利影响。本研究旨在评估氯化汞(HgCl)的生殖毒性后果。将五组性成熟的白化大鼠给予口服氯化汞(HgCl)处理。(G1)对照组接受生理盐水处理;(G2)(5.25毫克/千克HgCl,处理30天);(G3)(5.25毫克/千克HgCl,处理60天);(G4)(10.5毫克/千克HgCl,处理30天);(G5)(10.5毫克/千克HgCl,处理60天)。在接受HgCl处理的大鼠组中,激素水平、精子数量、精子活力、精子存活率以及包括体重在内的生殖器官重量均显著降低,而精子异常率则升高。分析表明,除了第2组(d = 0.59)和第3组(d = 0.18)的精子异常情况分别观察到中等和较小的效应量外,所有组中精子参数(包括精子数量、活力和存活率)的效应量(Cohen's d)都极高,这表明该干预对精子参数有显著影响。HgCl的给药导致睾丸中氧化应激的诱导,表现为脂质过氧化(MDA)大幅增强,同时在汞处理组的睾丸中,过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)和谷胱甘肽过氧化物酶(GPx)等抗氧化酶的活性大幅下降。与此同时,参与精子发生的基因,即睾丸中的热休克蛋白70(Hsp - 70)、胰岛素样生长因子(IGF)、谷胱甘肽 - S - 转移酶和p53的mRNA水平下调。抗凋亡蛋白B细胞淋巴瘤(Bcl - 2)的表达降低,相反,细胞增殖蛋白Ki - 67以剂量和时间依赖的方式增加。组织病理学研究显示,与对照组相比,睾丸、附睾、前列腺和精囊出现退行性变化。所有证据表明,汞暴露后,机体对自由基和抗氧化剂防御之间可能失衡,使睾丸更容易受到氧化损伤。这种失衡可能对男性生殖系统的功能产生不利影响。