Department of Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azhar University, Nasr City, Cairo, Egypt.
Food Chem Toxicol. 2010 Feb;48(2):572-8. doi: 10.1016/j.fct.2009.11.034. Epub 2009 Nov 14.
Nitrate is a common contaminant in groundwater aquifers. Current study aimed at evaluating the potential testicular toxicity of sodium nitrate in rats. Sodium nitrate was given orally to rats at doses of 50, 100 or 200 mg/kg/day for 60 consecutive days. Sperm count and motility, daily sperm production and testis weight were significantly decreased specially at high doses. Testicular activity of lactate dehydrogenase-X, glucose-6-phosphate dehydrogenase, and acid phosphatase were inhibited in a dose-related manner. Lipid peroxides and hydrogen peroxide production were significantly increased in all treated animals. This was accompanied by inhibition of testicular activities of superoxide dismutase and glutathione peroxidase. Fifty mg/kg of sodium nitrate did not significantly alter catalase or glutathione reductase activity. Glutathione was significantly decreased by sodium nitrate in a dose-related manner. The decrease in sperm count and motility and daily sperm production was confirmed by histopathological studies which indicated chromatolysis, pyknosis and necrosis in spermatocytes. In conclusion, subchronic exposure of rats to sodium nitrate results in testicular toxicity as evidenced by decreased sperm count and motility, daily sperm production and testis weight, inhibited activity of enzyme markers of spermatogenesis and induction of histopathological changes. These effects are attributed, at least partly, to testicular oxidative stress.
硝酸盐是地下水含水层中的一种常见污染物。本研究旨在评估亚硝酸钠对大鼠的潜在睾丸毒性。亚硝酸钠以 50、100 或 200mg/kg/天的剂量经口给予大鼠，连续 60 天。精子计数和活力、每日精子产量和睾丸重量均显著降低，尤其是高剂量时。乳酸脱氢酶-X、葡萄糖-6-磷酸脱氢酶和酸性磷酸酶的睾丸活性呈剂量依赖性抑制。所有处理动物的脂质过氧化物和过氧化氢生成均显著增加。这伴随着超氧化物歧化酶和谷胱甘肽过氧化物酶的睾丸活性抑制。50mg/kg 的亚硝酸钠对过氧化氢酶或谷胱甘肽还原酶的活性没有显著改变。谷胱甘肽含量随亚硝酸钠剂量呈剂量依赖性降低。精子计数和活力以及每日精子产量的减少通过组织病理学研究得到证实，该研究表明精母细胞出现了溶酶体、固缩和坏死。总之，大鼠亚慢性暴露于亚硝酸钠会导致睾丸毒性，表现为精子计数和活力、每日精子产量和睾丸重量降低，生精酶标记物活性抑制以及组织病理学变化诱导。这些影响至少部分归因于睾丸氧化应激。
