Adesiyan Adebukola C, Oyejola Titilola O, Abarikwu Sunny O, Oyeyemi Matthew O, Farombi Ebenezer O
Drug Metabolism and Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Nigeria.
Exp Toxicol Pathol. 2011 Mar;63(3):201-7. doi: 10.1016/j.etp.2009.11.008. Epub 2010 Jan 18.
The present study evaluated the possible protective effects of selenium against atrazine-induced toxicity in the liver and reproductive system of rats. Atrazine administered to rats orally at a dose of 120 mg/kg caused an inhibition in the activity of glutathione-S-transferase and an increase in malondialdehyde formation in the liver, testis and epididymis. Superoxide dismutase decreased in the liver and testis but was increased in the epididymis. Furthermore, hepatic glutathione and lactate dehydrogenase activity increased while epididymal catalase, ascorbate content, hepatic aspartate aminotransferase and glutathione peroxidase activities in all the tissues decreased in the atrazine-treated animals. Hepatic, testicular and epididymal alanine aminotransferase activities were not affected by atrazine (p>0.05). Decreased epididymal and testicular sperm number, sperm motility, daily sperm production and increased number of dead and abnormal sperm were observed in atrazine-treated rats. Treatment of rats orally with selenium at a dose of 0.25 mg/kg did not prevent atrazine-induced changes in sperm characteristics and had no protective effects against atrazine-induced biochemical alterations in the testis and epididymis except testicular lactate dehydrogenase. Catalase activity and ascorbate contents were unchanged in these groups of animals. However, selenium effectively protected against atrazine-induced changes in biochemical indices in the liver. In rats treated with selenium alone, glutathione peroxidase in all the tissues, hepatic glutathione and superoxide dismutase, testicular lactate dehydrogenase activity and ascorbate content increased, while hepatic catalase activities decreased (p<0.05). Our data suggest that selenium effectively attenuated the toxic effects of atrazine-induced liver changes but not in the reproductive organs and sperms of rats. Selenium might therefore be useful in ameliorating oxidative stress in the liver.
本研究评估了硒对大鼠肝脏和生殖系统中阿特拉津诱导的毒性的可能保护作用。以120 mg/kg的剂量给大鼠口服阿特拉津，导致肝脏、睾丸和附睾中谷胱甘肽-S-转移酶活性受到抑制，丙二醛形成增加。肝脏和睾丸中的超氧化物歧化酶减少，但附睾中的超氧化物歧化酶增加。此外，在阿特拉津处理的动物中，肝脏中的谷胱甘肽和乳酸脱氢酶活性增加，而附睾中的过氧化氢酶、抗坏血酸含量、肝脏中的天冬氨酸转氨酶和所有组织中的谷胱甘肽过氧化物酶活性均降低。肝脏、睾丸和附睾中的丙氨酸转氨酶活性不受阿特拉津影响（p>0.05）。在阿特拉津处理的大鼠中，观察到附睾和睾丸中的精子数量、精子活力、每日精子产量减少，死精子和异常精子数量增加。以0.25 mg/kg的剂量给大鼠口服硒，除睾丸乳酸脱氢酶外，并未预防阿特拉津诱导的精子特征变化，对阿特拉津诱导的睾丸和附睾生化改变也没有保护作用。这些动物组中的过氧化氢酶活性和抗坏血酸含量没有变化。然而，硒有效预防了阿特拉津诱导的肝脏生化指标变化。在单独用硒处理的大鼠中，所有组织中的谷胱甘肽过氧化物酶、肝脏中的谷胱甘肽和超氧化物歧化酶、睾丸中的乳酸脱氢酶活性和抗坏血酸含量增加，而肝脏中的过氧化氢酶活性降低（p<0.05）。我们的数据表明，硒有效减轻了阿特拉津诱导的肝脏变化的毒性作用，但对大鼠的生殖器官和精子没有作用。因此，硒可能有助于改善肝脏中的氧化应激。
