Venkataraman Prabhu, Muthuvel Raju, Krishnamoorthy Gunasekaran, Arunkumar Arumugam, Sridhar Muthusami, Srinivasan Narasimhan, Balasubramanian Karundevi, Aruldhas Maria Michael, Arunakaran Jagadeesan
Department of Endocrinology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai 600113, India.
Neurotoxicology. 2007 May;28(3):490-8. doi: 10.1016/j.neuro.2006.11.002. Epub 2006 Dec 1.
PCBs are one of the environmental toxicants and neurotoxic compounds which induce the production of free radicals leading to oxidative stress. Oxidative stress is a contributing factor to alteration caused in neurodegenerative processes. The ability of Vitamin C to retard oxidative processes has been recognized for many years. Therefore, the present experiment was carried out to determine the antioxidant role of ascorbate on Aroclor 1254 induced oxidative stress in brain regions of albino rats. One group of rats received corn oil as vehicle for 30 days as control. The other group of rats were administered Aroclor 1254 at a dose of 2 mg/kg bw/day intraperitoneally for 30 days. One group of rats received Vitamin C (100 mg/kg bw/day) orally simultaneously with Aroclor 1254 for 30 days. The brain was dissected to cerebral cortex (Cc), cerebellum (C) and hippocampus (H). Enzymatic and non-enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), reduced glutathione (GSH) and Vitamin C were estimated. Hydrogen peroxide (H(2)O(2)), lipid peroxidation (LPO) and acetylcholine esterase activity (AchE) were determined. Activities of SOD, CAT, GPx, GST, AchE and the concentration of GSH, Vitamin C were decreased while an increase in H(2)O(2) and LPO were observed in brain regions of PCB treated animals. Vitamin C administration retrieved all the parameters except GST, significantly. These results suggest that PCB induces oxidative stress in rat brain by decreasing the activities of antioxidant enzymes, which can be protected by Vitamin C treatment.
多氯联苯是环境毒物和神经毒性化合物之一,可诱导自由基产生,导致氧化应激。氧化应激是神经退行性过程中发生改变的一个促成因素。多年来,维生素C抑制氧化过程的能力已得到认可。因此,本实验旨在确定抗坏血酸盐对白化病大鼠脑区中Aroclor 1254诱导的氧化应激的抗氧化作用。一组大鼠接受玉米油作为载体,持续30天作为对照。另一组大鼠腹腔注射Aroclor 1254,剂量为2 mg/kg体重/天,持续30天。一组大鼠在接受Aroclor 1254的同时口服维生素C(100 mg/kg体重/天),持续30天。将大脑解剖为大脑皮层(Cc)、小脑(C)和海马体(H)。对超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽-S-转移酶(GST)、还原型谷胱甘肽(GSH)和维生素C等酶促和非酶促抗氧化剂进行了评估。测定了过氧化氢(H₂O₂)、脂质过氧化(LPO)和乙酰胆碱酯酶活性(AchE)。在多氯联苯处理动物的脑区中,SOD、CAT、GPx、GST、AchE的活性以及GSH、维生素C的浓度均降低,而H₂O₂和LPO则升高。维生素C给药后,除GST外,所有参数均有显著恢复。这些结果表明,多氯联苯通过降低抗氧化酶的活性在大鼠脑中诱导氧化应激,而维生素C治疗可对其起到保护作用。