Zaidi S M Kashif R, Banu Naheed
Department of Biochemistry, Faculty of Life Sciences, A.M.U. 202002, Aligarh, India.
Clin Chim Acta. 2004 Feb;340(1-2):229-33. doi: 10.1016/j.cccn.2003.11.003.
Stress is known to affect synaptic plasticity, dendritic morphology and induces neurotoxic damage in humans, probably through generation of free radicals. Both ex vivo antioxidant vitamins and in vivo free radical scavenging enzymes exist. In the present study, restraint stress induced pro-oxidant status of rat brain was evaluated in terms of measurement of glutathione (GSH), lipid peroxidation (thiobarbituric acid reactive substances, TBARS) and free radical scavenging enzymes activities. The efficacy of antioxidant vitamins A, E and C alone and in combination was also evaluated in modulating inherent antioxidant system in stressed rats.
Rats were treated with vit A, E and C alone (15 mg/kg of body weight) and in combination vitamins (E and C) prior to and after 6 h of restraint stress exposure. Both nonstressed and stressed rats were handled simultaneously. Pro-oxidant status of brain tissue was evaluated by determining the levels of GSH, TBARS and activities of superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT).
Restraint stress induced a decrease in the level of GSH and the activities of SOD, GST and catalase, while the levels of TBARS were found elevated. Both pre-stress and post-stress vitamin treatments (either alone or combined) resulted in alteration of these parameters towards their controls values with a relative dominance by latter. Vitamin E was found most effective in restoring inherent antioxidant system, no additive effect was observed in combined vitamin treatment as expected.
Immobilization of rats generated oxidative stress in rat brain, by decreasing the activities of SOD, GST, catalase and glutathione levels, while increasing the lipid peroxidation. Post stress vitamin E treatment was found most effective than vitamins A and C in enhancing the levels of glutathione and activities of SOD, GST and catalase and decreasing lipid peroxidation. Thus vitamin E can be given as a nutritional supplement for scavenging free radical generated in the brain tissues in order to reduce oxidative stress.
已知压力会影响突触可塑性、树突形态，并可能通过自由基的产生在人类中诱导神经毒性损伤。体外抗氧化维生素和体内自由基清除酶均存在。在本研究中，通过测量谷胱甘肽（GSH）、脂质过氧化（硫代巴比妥酸反应性物质，TBARS）和自由基清除酶活性，评估了束缚应激诱导的大鼠脑促氧化状态。还评估了抗氧化维生素A、E和C单独及联合使用在调节应激大鼠固有抗氧化系统方面的功效。
在束缚应激暴露6小时之前和之后，用维生素A、E和C单独（15毫克/千克体重）以及联合维生素（E和C）对大鼠进行处理。非应激和应激大鼠同时进行处理。通过测定GSH水平、TBARS水平以及超氧化物歧化酶（SOD）、谷胱甘肽-S-转移酶（GST）和过氧化氢酶（CAT）的活性，评估脑组织的促氧化状态。
束缚应激导致GSH水平以及SOD、GST和过氧化氢酶的活性降低，而TBARS水平升高。应激前和应激后的维生素处理（单独或联合）均导致这些参数朝着对照值改变，且后者相对占优势。发现维生素E在恢复固有抗氧化系统方面最有效，联合维生素处理未观察到预期的相加效应。
大鼠固定导致大鼠脑产生氧化应激，表现为SOD、GST、过氧化氢酶活性和谷胱甘肽水平降低，同时脂质过氧化增加。发现应激后维生素E处理在提高谷胱甘肽水平以及SOD、GST和过氧化氢酶活性并降低脂质过氧化方面比维生素A和C更有效。因此，维生素E可作为营养补充剂给予，以清除脑组织中产生的自由基，从而减轻氧化应激。
