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镉的氧化应激介导的神经毒性。

Oxidative stress-mediated neurotoxicity of cadmium.

作者信息

Kumar R, Agarwal A K, Seth P K

机构信息

Industrial Toxicology Research Centre, Lucknow, India.

出版信息

Toxicol Lett. 1996 Dec;89(1):65-9. doi: 10.1016/s0378-4274(96)03780-0.

DOI:10.1016/s0378-4274(96)03780-0
PMID:8952713
Abstract

Young albino rats were administered cadmium i.p. (0.4 mg/kg body weight) for a period of 30 days and membrane fluidity, intracellular calcium level, MDA level, phospholipids, (phosphatidylethanolamine, phosphatidylcholine, phosphatidylinositol, phosphatidylserine and sphingomyelin) and reduced glutathione were studied in olfactory bulb, cerebellum and rest of brain. A decrease in membrane fluidity was observed in all the brain regions studied, maximum being in olfactory bulb (21%). Intracellular calcium (Ca+2)i level was increased significantly in olfactory bulb (150%) followed by rest of brain (98%) and cerebellum (71%) in Cd-exposed rats in comparison with controls. A significant decrease in phosphatidylcholine (27%) and phosphatidylethanolamine (22%) was observed in olfactory bulb, while other phospholipids remained unaffected. TBA reactivity was increased in olfactory bulb (77%), cerebellum (35%) and rest of brain (27%). Reduced glutathione level was also decreased in different brain regions. The results suggest that the effect of cadmium in brain is region-specific and most pronounced in olfactory bulb.

摘要

给幼年白化大鼠腹腔注射镉(0.4毫克/千克体重),持续30天,然后研究嗅球、小脑和大脑其他部分的膜流动性、细胞内钙水平、丙二醛水平、磷脂(磷脂酰乙醇胺、磷脂酰胆碱、磷脂酰肌醇、磷脂酰丝氨酸和鞘磷脂)以及还原型谷胱甘肽。在所研究的所有脑区均观察到膜流动性降低,其中嗅球降低最多(21%)。与对照组相比,镉暴露大鼠的嗅球细胞内钙(Ca+2)i水平显著升高(150%),其次是大脑其他部分(98%)和小脑(71%)。嗅球中的磷脂酰胆碱(27%)和磷脂酰乙醇胺(22%)显著减少,而其他磷脂未受影响。嗅球、小脑和大脑其他部分的硫代巴比妥酸反应性分别升高了77%、35%和27%。不同脑区的还原型谷胱甘肽水平也降低。结果表明,镉对大脑的影响具有区域特异性,在嗅球中最为明显。

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