Bandhu H K, Dani Vijayta, Garg M L, Dhawan D K
Department of Biophysics, Panjab University, Chandigarh, India.
Drug Chem Toxicol. 2006 Jan;29(1):11-24. doi: 10.1080/01480540500408507.
The current study was designed to evaluate the hepatoprotective role of zinc after lead (Pb) treatment of protein-deficient (PD) rats. The animals were subjected to seven different treatment groups: G-1 (normal control, 18% protein), G-2 (protein-deficient, 8% protein), G-3 (Pb-treated, 100 mg/kg body weight of lead acetate), G-4 (Zn-treated, zinc sulfate at a dose level of 227 mg/L drinking water), G-5 (PD + Pb-treated), G-6 (PD + Zn-treated), and G-7 (PD + Pb + Zn-treated). Serum albumin levels and total serum protein contents were estimated to assess the severity of protein deficiency at the end of 8 weeks in all the treatment groups. Also, the study explored the role of zinc on antioxidative defense system enzymes in liver of protein-deficient rats subjected to lead toxicity treatment. Further, the study was extended to elucidate the levels of zinc and lead in liver tissue after different treatments of rats using positron-induced X-ray emission technique (PIXE). The current study indicated a significant change in the levels of various antioxidative enzymes and serum albumin as well as total protein contents of protein-deficient rats subjected to lead treatment. A significant increase in the levels of malondialdehyde (MDA), catalase, and glutathione peroxidase (GPx) was seen after 8 weeks of lead treatment of protein-deficient rats. On the contrary, levels of albumin, total protein content, superoxide dismutase (SOD), GSH, were found to be decreased. Interestingly, zinc supplementation has tended to normalize the altered levels of these enzymes to a significant extent. The levels of zinc in liver tissue was found to be decreased significantly in protein-deficient as well as lead-treated rats. However, hepatic zinc concentration was increased to a significant extent in protein-deficient rats supplemented with zinc when compared with protein-deficient rats. Further, the presence of lead was also observed in livers of lead-treated animals. In conclusion, the study revealed the antioxidative role of zinc in hepatotoxic conditions induced by subjecting the rats to protein-deficient diet and lead treatment.
本研究旨在评估锌对蛋白质缺乏(PD)大鼠铅(Pb)处理后的肝脏保护作用。将动物分为七个不同的治疗组:G-1(正常对照,18%蛋白质)、G-2(蛋白质缺乏,8%蛋白质)、G-3(铅处理,100mg/kg体重醋酸铅)、G-4(锌处理,硫酸锌剂量为227mg/L饮用水)、G-5(PD+铅处理)、G-6(PD+锌处理)和G-7(PD+铅+锌处理)。在所有治疗组8周结束时,评估血清白蛋白水平和血清总蛋白含量,以评估蛋白质缺乏的严重程度。此外,该研究探讨了锌对遭受铅毒性处理的蛋白质缺乏大鼠肝脏中抗氧化防御系统酶的作用。进一步地,该研究扩展到使用正电子诱导X射线发射技术(PIXE)来阐明大鼠不同处理后肝脏组织中锌和铅的水平。本研究表明,遭受铅处理的蛋白质缺乏大鼠的各种抗氧化酶水平、血清白蛋白以及血清总蛋白含量发生了显著变化。蛋白质缺乏大鼠经铅处理8周后,丙二醛(MDA)、过氧化氢酶和谷胱甘肽过氧化物酶(GPx)水平显著升高。相反,白蛋白水平、总蛋白含量、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)水平则降低。有趣的是,补充锌已在很大程度上使这些酶的改变水平趋于正常。蛋白质缺乏以及经铅处理的大鼠肝脏组织中的锌水平显著降低。然而,与蛋白质缺乏大鼠相比,补充锌的蛋白质缺乏大鼠肝脏锌浓度显著增加。此外,在经铅处理的动物肝脏中也观察到铅的存在。总之,该研究揭示了锌在大鼠因蛋白质缺乏饮食和铅处理诱导的肝毒性条件下的抗氧化作用。