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作 者:梁骏华[1] 钟玉芳[1] 戴中华[1] 石年[1]
机构地区:[1]华中科技大学同济医学院公共卫生学院卫生毒理系
出 处:《癌变.畸变.突变》2006年第3期218-220,共3页Carcinogenesis,Teratogenesis & Mutagenesis
摘 要:背景与目的:研究1,1-双(4-氯苯)-2,2,2-三氯乙烷(DDT)对大鼠大脑皮层、海马和小脑组织诱导的氧化应激作用。材料与方法:SD大鼠共24只,随机分为4组,即溶剂对照组与低(20mg/kg)、中(40mg/kg)、高(80mg/kg)3个DDT剂量组,每组6只,大鼠经口灌胃染毒7d后断头处死,测定大脑皮层、海马和小脑组织丙二醛(MDA)水平和总超氧化物歧化酶(T-SOD)、谷胱甘肽过氧化物酶(GSH-PX)和谷胱甘肽还原酶(GR)活力。结果:①与溶剂对照组比较,随着DDT浓度的增加,大鼠大脑皮层、海马和小脑中MDA含量升高,T-SOD活性下降;②大脑皮层GSH-PX活性在低剂量时升高,在中、高剂量组则显著下降,海马GSH-PX活性随着剂量的增加而显著下降,而小脑GSH-PX活性则在中、高剂量组出现显著下降;③海马GR活性在中、高剂量组随着剂量的增加而显著下降,在小脑则只有高剂量组出现了下降,皮层GR活性在各剂量组未观察到明显改变。结论:DDT可以引发神经组织的脂质过氧化反应增强。DDT导致机体组织的氧化损伤可能在动物神经毒性中起重要作用。BACKGROUND & AIM:To study the oxidative stress induced by 1, 1-Bis(4-chlorophenyl) -2, 2,2-trichloroethane (DDT) in the cerebral cortex, hippocampus and cerebellum of rats.MATERIAL AND METHODS:24 Sprague-Dawley male rats were randomly divided into four groups with 6 rats in each: solvent control, low (20 mg/kg),moderate(40 mg/ kg) and high(80 mg/ kg) dose groups. Test substances were administered by gavage and rats weresacrificed 7 days after treatment. Malonyldialdehyde (MDA), total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-PX) and glutathion reductase (GR) in cerebral cortex, hippocampus and cerebellum were examined.RESULTS:① Compared with the solvent control, with the dose increased, the content of MDA in cerebral cortex,hippocampus and cerebellum significantly increased while T-SOD activity decreased significantly. ②GSH-PX activity of cerebral cortex significantly increased at low dose group, but significantly decreased at moderate and high dose groups(P〈0.05) . In hippocampus and cerebellum, with the dose increased GSH-PX activity decreased significantly. ③ GR activity of hippocampus decreased significantly at moderate dose and high dose groups(P 〈0.05). In cerebellum ,it only decreased at high dose group(P 〈0.05) . In cerebral cortex, the alteration of GR activity in different dose groups was not observed. CONCLUSION: DDT could induce oxidative stress in nervous tissue. The tissue oxidative damage might be one of the primary mechanisms of neurotoxicity of DDT.
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