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维生素E对三氯乙烯急性染毒大鼠肝脏脂质过氧化与抗氧化酶的影响 被引量:2

Effect of Vitamin E on Lipid Peroxidation and Antioxidase Activity in the Liver of Rats Acutely Exposed to Trichloroethylene
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摘要 本文用抗氧化剂维生素E 预处理后,观察了三氯乙烯(3000mgkg B- W-) 一次性经口染毒24h 大鼠肝脏的超氧化物歧化酶、谷胱甘肽过氧化物酶等抗氧化酶活力及丙二醛含量的变化,结果表明三氯乙烯染毒组肝脏中丙二醛含量、超氧化物歧化酶活力及血清谷丙转氨酶、谷草转氨酶活力均高于对照组(P< 0-01) ;而维生素E 干预组的丙二醛含量、超氧化物歧化酶活力及血清谷丙转氨酶、谷草转氨酶活力均分别低于三氯乙烯染毒组(P< 0-01) ,说明三氯乙烯急性染毒可引起肝脏脂质过氧化反应及肝损害,肝脏超氧化物歧化酶活力升高可能是机体受自由基及脂质过氧化反应刺激而诱导产生的一种适应性反应,维生素E 对三氯乙烯所致的肝损害有一定的保护作用。 After single oral administration of trichloroethylene (3000mg/kg B.W.), the serum and liver were colletted. The activity of serum GPT and GOT(as indices of liver damage) were measured. Also, The activity of superoxide dismutase(SOD)、glutathione peroxidase(GSH-Px) and the level of malondialdehyde(MDA) were analysed in the liver homogenate of the rats. The results revealed the activity of liver SOD and serum GPT、GOT in the rats acutely exposed to trichlorothylene(TCE) was significantly higher than that of those the control (P<0 01). Pretreatment with vitamin E.could reduce the level of liver MDA and the activity of liver SOD、 serum GPT and GOT. It suggested that TCE might induce lipid peroxidation in the liver of rats and vitamine E could protect liver from TCE-induced liver damage in some degree.
出处 《中国实验动物学杂志》 1999年第3期129-132,共4页 Chinese Journal of Laboratory Animal Science
关键词 染毒 肝脏 三氯乙烯 超氧化物歧化酶活力 维生素E 转氨酶 鼠肝 丙二醛含量 抗氧化酶活力 经口 Vitamin E Trichloroethylene(TCE) poisoning rats Malondialdehyde(MDA) Superoxide dismutase(SOD) Glutathione peroxidase(GSH-Px)
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  • 1李长生,高建飞,潘显光,李清泉.肺癌患者血清Mn-SOD和LSA对比观察[J].肿瘤防治研究,1994,21(3):146-147. 被引量:1
  • 2Nordberg GF. Application of the critical effect and critical concentration concept to human risk assessment[A]. In: cadmium in the Human Enviroment, Toxicity and Carcinogencity [ R]. Lyon: IARC, 1992.
  • 3Chin TA, Templeton DM. Effects of CdCl2 and Cd-metallothionein on cultured mesangial cells[J]. Toxicol Appl Pharmacol, 1992,116( 1 ): 133-141.
  • 4Thevenod F, Friedmann JM, Katsen AD, et al. Up-regulation of multidrug resistance P-glycoprotein via nuclear factor-kappaB activation protects kidney proximal tubule cells from cadmium and reactive oxygen species-induced apoptosis[J] .J Biol Chem,2000,275
  • 5Gennari A, Cortese E, Boveri M, et al. Sensitive endpoints for evaluating cadmium-induced acute toxicity in LLC-PK1 cells[ J]. Toxicol,2003,183 ( 1-3) :211-220.
  • 6Karmaker R, Banik S,Bandyopadhyay S,et al. Cadmium induced alteration of hepatic lipid peroxidation, glutathione S-transferase activity and reduced glutathione level and their possible correlation with chromosomal abberration in mice, a time course study[
  • 7Williams PD.The application of renal cells in culture in studying drug-induced nephrotoxicity[ J]. In Vitro Cell Der Biol, 1989,25(9) :800-805.
  • 8Hori R, Yamamoto K, Saito H. Effect of aminoglycoside antibiofcs on cellular functions of kidney epithelial cell line ( LLC-PK1 ): a model system for aminoglycoside nephrotoxicity[J]. J Pharmacol Exper Therapeutics, 1984,230(2) :742-748.
  • 9Manca D,Ricard AC,Trottier B,et al. Studies on lipid peroxidation in rat tissues following administration of low and moderate doses of cadmium chloride[J]. Toxicol, 1991,67(3): 303-323.
  • 10Blasiak J,Trzeciak A, Dziki A, et al. Synergistic effect of vitamin C on DNA damage induced by cadmium [ J ]. Gen Physiol Biophys, 2000,19 (4): 373-379.

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