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首页> 外文期刊>Neurochemical Research >Augmentation of Aluminum-Induced Oxidative Stress in Rat Cerebrum by Presence of Pro-oxidant (Graded Doses of Ethanol) Exposure
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Augmentation of Aluminum-Induced Oxidative Stress in Rat Cerebrum by Presence of Pro-oxidant (Graded Doses of Ethanol) Exposure

机译:存在前氧化剂(乙醇的分级剂量)暴露可增强铝诱导的大鼠脑氧化应激

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摘要

Both aluminum and ethanol are pro-oxidants and neurotoxic. Considering the possibilities of co-exposure and sharing mechanisms of producing neurotoxicity, the present study was planned to identify the level of aluminum-induced oxidative stress in altered pro-oxidant (ethanol exposure) status of cerebrum. Male rats were coexposed to aluminum and ethanol for 4 weeks. After the exposure period, cerebral levels of protein, reduced glutathione (GSH), lipid peroxidation (TBARS) were measured. Activities of catalase, superoxide dismutase (SOD), glutathione reductase (GR) and glutathione perioxidase (GPx) of cerebrum were estimated. In most of the cases significant correlations were observed between the alterations and graded ethanol doses, suggesting a dose-dependency in pushing the oxidant equilibrium toward pro-oxidants. Aluminum is found to influence significantly all the studied parameters of oxidative stress. Likewise, ethanol also influenced these parameters significantly, except GR, while the interaction between ethanol and aluminum could significantly influence only the GSH content and GR activity of cerebrum. Present study demonstrate that coexposure of aluminum with pro-oxidant might favor development of aluminum-induced oxidative stress in cerebrum. This observation might be helpful in understanding of mechanism of neurodegenerative disorders and ameliorate them.
机译:铝和乙醇都是促氧化剂和神经毒性。考虑到共同暴露和产生神经毒性的共享机制的可能性,本研究计划确定在铝的改变前氧化剂(乙醇暴露)状态下铝诱导的氧化应激水平。将雄性大鼠与铝和乙醇共同暴露4周。暴露期后,测量大脑的蛋白质水平,还原型谷胱甘肽(GSH),脂质过氧化(TBARS)。评估了过氧化氢酶,超氧化物歧化酶(SOD),谷胱甘肽还原酶(GR)和谷胱甘肽过氧化物酶(GPx)的活性。在大多数情况下,在变化和分级乙醇剂量之间观察到显着的相关性,这表明将氧化剂平衡推向促氧化剂时存在剂量依赖性。发现铝对所有研究的氧化应激参数有显着影响。同样,除GR外,乙醇也对这些参数有显着影响,而乙醇和铝之间的相互作用仅对GSH含量和大脑GR活性有显着影响。目前的研究表明铝与前氧化剂的共同暴露可能有利于铝诱导的大脑氧化应激的发展。该观察结果可能有助于理解神经退行性疾病的机制并改善它们。

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