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亚慢性暴露后大鼠脑组织中抗氧化酶和谷胱甘肽在3,3',4,4',5-五氯联苯(PCB 126)诱导的氧化应激中的作用评估

Assessment of the roles of antioxidant enzymes and glutathione in 3,3',4,4',5-Pentachlorobiphenyl (PCB 126)-induced oxidative stress in the brain tissues of rats after subchronic exposure.

作者信息

Hassoun Ezdihar A, Periandri-Steinberg Seanna

机构信息

College of Pharmacy, University of Toledo, Toledo, OH 43606, U.S.A.

出版信息

Toxicol Environ Chem. 2010 Feb 1;92(2):301. doi: 10.1080/02772240902846660.

Abstract

The abilities of various doses of 3,3',4,4',5-pentachlorobiphenyl (PCB126) to induce changes in antioxidant enzyme activities and glutathione levels in the brain tissues of rats were examined in rats after subchronic exposure. Groups of rats were administered 10,30, 100, 300, 550 or 1000 ng PCB 126/kg/day, p.o., for 13 weeks and the activities of supeoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), as well as (GSH) levels were determined in the brain tissue homogenates. Treatment resulted in significant and dose-dependent increases in the activities of the three tested enzymes. While maximal increase GSH-Px activity was achieved with a dose of 100-175 mg/kg/day, CAT and SOD activities continued to increase in response to maximal dose used for this study. GSH levels on the other hand, were suppressed significantly in a dose-dependent fashion. Data suggest that previously observed increase in oxidative stress production by PCB-126 in the brain tissues of rats is associated with dose-dependent rise in antioxidant enzyme activities and GSH depletion. However, the increases in the antioxidant enzyme activities can not provide full protection against oxidative damage induced by the same doses. In addition, GSH depletion plays a critical role in the previously observed oxidative stress in response to this compound.

摘要

在亚慢性暴露后的大鼠中,研究了不同剂量的3,3',4,4',5-五氯联苯(PCB126)对大鼠脑组织抗氧化酶活性和谷胱甘肽水平变化的诱导能力。将大鼠分组,经口给予10、30、100、300、550或1000 ng PCB 126/kg/天,持续13周,并测定脑组织匀浆中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)的活性以及谷胱甘肽(GSH)水平。处理导致三种受试酶的活性显著且呈剂量依赖性增加。虽然剂量为100 - 175 mg/kg/天时GSH-Px活性达到最大增加,但CAT和SOD活性在本研究使用的最大剂量下仍持续增加。另一方面,GSH水平以剂量依赖性方式显著降低。数据表明,先前观察到的PCB - 126在大鼠脑组织中产生的氧化应激增加与抗氧化酶活性的剂量依赖性升高和GSH消耗有关。然而,抗氧化酶活性的增加不能完全保护免受相同剂量诱导的氧化损伤。此外,GSH消耗在先前观察到的对该化合物的氧化应激中起关键作用。

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