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乙酰半胱氨酸对铅致大鼠肾脏皮质氧化损伤的保护效应 被引量:4

N-acetyl cysteine protects from oxidative damage of kidney cortex in rats from exposed to lead
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摘要 采用饮水对大鼠进行铅染毒(300mg/L)和NAC保护(Pb 300mg/L+NAC 1g/L)试验,为期8周,通过检测肾皮质中抗氧化指标和微量元素含量变化及超微结构来探讨铅对肾的毒性损伤及NAC的保护效应。结果表明,与对照组比较,铅染毒组及NAC保护组肾皮质中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和还原型谷胱甘肽(GSH)含量显著或极显著降低(P<0.05或P<0.01),丙二醛(MDA)含量显著或极显著升高(P<0.05或P<0.01),肾皮质中锰(Mn)、锌(Zn)、硒(Se)含量显著降低(P<0.05)。与染毒组比较,NAC保护组肾皮质SOD、GSH-Px活性和GSH含量显著升高(P<0.05);肾皮质Mn、Se含量显著升高(P<0.05)。超微结构观察发现,铅染毒使肾皮质中细胞核染色质边集,有大量畸形核,线粒体肿胀变形,部分嵴断裂,溶解;NAC保护组损伤变化轻微。表明NAC对铅暴露所致肾毒性损伤具有一定的保护效应。 Lead acetate(300 mg Pb/L) and/or NAC(1 g NAC/L) were administered as drinking water to rats for eight weeks.Antioxidant indices,contents of trace elements and ultrastructure were detected to investigate the toxicological effects of lead on the kidney of rats and the protective effect of NAC.The results indicated that activities of superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px),contents of glutathione(GSH) in the lead group and lead-NAC group were significantly lower than those in the control group(P0.05 or P0.01).Meanwhile,contents of malondialdehyde(MDA) in these exposed groups increased remarkably(P0.05 or P0.01),contents of manganese,zinc and selenium were significantly dereseased.Activities of SOD and GSH-Px,contents of GSH in the NAC group were significantly higher than those of the lead groups;the contents of manganese and selenium in the NAC group were significantly increased(P0.05).Ultrastructurally,nucleoli damaged with crush and salvation,mitochondria damaged with swelling,disappearance and fragmentation of carina following exposed to lead were observed.The pathological changes in the NAC group were not obvious.It indicated that NAC could reduce lipid peroxidation and has protective effect on lead-induced nephrotoxicity.
出处 《中国兽医学报》 CAS CSCD 北大核心 2011年第1期99-102,106,共5页 Chinese Journal of Veterinary Science
基金 江苏省高校"青蓝工程"中青年学术带头人培养对象资助项目(2006) 江苏省自然科学基金资助项目(BK2008214)
关键词 大鼠 肾脏皮质 乙酰半胱氨酸 脂质过氧化 微量元素 SD rat kidney cortex lead N-acetyl cysteine lipid peroxidation trace element
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