King Faisal University, College of Science, Department of Biological Sciences, Al-Hufof, Ahsaa, Saudi Arabia.
King Faisal University, College of Science, Department of Biological Sciences, Al-Hufof, Ahsaa, Saudi Arabia and University of Alexandria, Faculty of Science, Department of Zoology, Alexandria, Egypt.
Histol Histopathol. 2014 Jan;29(1):45-55. doi: 10.14670/HH-29.45. Epub 2013 Jun 10.
The present study was carried out to investigate (1) the alterations in biochemical parameters, free radicals and enzyme activities induced by aluminum chloride (AlCl₃) in kidney of male Swiss albino mice, and (2) the role of taurine in alleviating the nephrotoxic effects of AlCl₃. Taurine plays an important role as an antioxidant and is consequently expected to protect tissues from damage caused by reactive oxygen metabolites.The animals were randomized into four groups (n=6/group). Group I was the control group. Group II received a single dose of AlCl₃ (25 mg Al³⁺/kg b.w, ip). Group III received taurine (100 mg/kg b.w., ip) for 5 consecutive days before administration of AlCl₃ (25 mg Al³⁺/kg b.w, ip). Group IV received taurine (100 mg/kg b.w., ip) for 5 consecutive days. 24 h following the administration of compounds, all the mice were assessed using serum and tissue homogenate biomarkers as well as the pathological evaluation. Exposure to AlCl₃ led to an increased level of renal lipid peroxidation as measured by malondialdehyde (MDA), while reduced glutathione (GSH), glutathione peroxidase (GPx) and catalase (CAT) decreased. Marked elevation of blood urea and serum creatinine concentrations were also observed in AlCl₃ treated mice, thereby indicating renal damage. All these factors were significantly improved by taurine pretreatment. The histological and ultrastructural observations on the kidney tissues also confirmed the renoprotective nature of taurine. Thus these results may indicate that taurine treatment protects against functional, biochemical and morphological damage in AlCl₃-induced acute renal failure in mice.
本研究旨在探讨（1）氯化铝（AlCl₃）对雄性瑞士白化小鼠肾脏中生化参数、自由基和酶活性的改变，以及（2）牛磺酸在缓解 AlCl₃肾毒性中的作用。牛磺酸作为一种抗氧化剂发挥着重要作用，因此有望保护组织免受活性氧代谢物的损伤。
动物随机分为四组（每组 n=6）。第 I 组为对照组。第 II 组单次给予 AlCl₃（25 mg Al³⁺/kg b.w，ip）。第 III 组在给予 AlCl₃（25 mg Al³⁺/kg b.w，ip）前连续 5 天给予牛磺酸（100 mg/kg b.w，ip）。第 IV 组连续 5 天给予牛磺酸（100 mg/kg b.w，ip）。给予化合物 24 h 后，所有小鼠均采用血清和组织匀浆生物标志物以及病理评估进行评估。
暴露于 AlCl₃导致肾脂质过氧化水平升高，丙二醛（MDA）测定值升高，而还原型谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GPx）和过氧化氢酶（CAT）降低。在 AlCl₃处理的小鼠中，还观察到血尿素和血清肌酐浓度显著升高，表明肾脏损伤。牛磺酸预处理显著改善了所有这些因素。对肾脏组织的组织学和超微结构观察也证实了牛磺酸的肾保护作用。因此，这些结果可能表明，牛磺酸治疗可防止 AlCl₃诱导的急性肾衰竭小鼠的功能、生化和形态损伤。
