Goel Ajay, Dani Vijayta, Dhawan D K
Department of Biophysics, Panjab University, Sector 14, Chandigarh 160014, India.
Chem Biol Interact. 2005 Oct 20;156(2-3):131-40. doi: 10.1016/j.cbi.2005.08.004.
The present study investigated the hepatoprotective role of zinc in attenuating the toxicity induced by chlorpyrifos in rat liver. Male Sprague-Dawley (SD) rats received either oral chlorpyrifos (13.5mg/kg body weight), zinc alone (227mg/l in drinking water) or combined chlorpyrifos plus zinc treatment for a total duration of 8 weeks. The effects of these treatments were studied on various parameters in rat liver, including lipid peroxidation, antioxidant enzymes, levels of metallothionein (MT) and hepatic histoarchitecture. Chlorpyrifos treatment resulted in a significant increase in hepatic lipid peroxidation and activities of superoxide dismutase (SOD), glutathione peroxidase (G-Px) and glutathione reductase (GR). On the contrary, chlorpyrifos intoxication caused a significant inhibition in the levels of reduced glutathione (GSH), catalase (CAT) and glutathione-S-transferase (GST) activities. However, zinc treatment to chlorpyrifos-intoxicated animals normalized the otherwise raised levels of lipid peroxidation to within normal limits. Moreover, zinc treatment to these animals resulted in an elevation in the levels of GSH, catalase and GST, as well as a significant decrease in the levels of SOD. Levels of MT were also found to be depressed in chlorpyrifos-treated animals, but tended to increase following co-administration of zinc. Additionally, chlorpyrifos-treated animals demonstrated increased vacuolization, necrosis and ballooning of the hepatocytes and dilatation of sinusoids as well as increase in the number of binucleated cells. However, zinc administration to chlorpyrifos-treated animals resulted in overall improvement in the hepatic histoarchitecture, emphasizing the protective potential of zinc. Hence, the present study suggests the protective potential of zinc in alleviating the hepatic toxicity induced by chlorpyrifos.
本研究调查了锌在减轻毒死蜱对大鼠肝脏诱导的毒性方面的肝脏保护作用。雄性斯普拉格-道利（SD）大鼠接受口服毒死蜱（13.5mg/kg体重）、单独补锌（饮用水中227mg/l）或毒死蜱加锌联合处理，总时长为8周。研究了这些处理对大鼠肝脏各种参数的影响，包括脂质过氧化、抗氧化酶、金属硫蛋白（MT）水平和肝脏组织结构。毒死蜱处理导致肝脏脂质过氧化以及超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（G-Px）和谷胱甘肽还原酶（GR）活性显著增加。相反，毒死蜱中毒导致还原型谷胱甘肽（GSH）、过氧化氢酶（CAT）水平以及谷胱甘肽-S-转移酶（GST）活性显著抑制。然而，对毒死蜱中毒动物进行锌处理可将原本升高的脂质过氧化水平恢复至正常范围。此外，对这些动物进行锌处理导致GSH、过氧化氢酶和GST水平升高，同时SOD水平显著降低。在毒死蜱处理的动物中还发现MT水平降低，但在联合补锌后有升高趋势。此外，毒死蜱处理的动物表现出肝细胞空泡化、坏死和气球样变增加，以及肝血窦扩张和双核细胞数量增加。然而，对毒死蜱处理的动物给予锌可使肝脏组织结构总体改善，突出了锌的保护潜力。因此，本研究表明锌在减轻毒死蜱诱导的肝脏毒性方面具有保护潜力。
