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首页> 外文期刊>Toxicological & Environmental Chemistry >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
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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

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

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摘要

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 after subchronic exposure. Groups of rats were administered 10, 30, 100, 300, 550, or 1000 ng PCB 126 kg−1 day−1, p.o., for 13 weeks and the activities of supeoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), as well as glutathione (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 in GSH-Px activity was achieved with a dose of 100-175 mg kg−1 day−1, CAT and SOD activities continued to increase in response to maximal dose used for this study. On the other hand, GSH levels 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 cannot 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.
机译:亚慢性暴露后,检查了不同剂量的3,3,4,4,5,5-五氯联苯(PCB126)诱导大鼠脑组织中抗氧化酶活性和谷胱甘肽水平变化的能力。每组大鼠分别接受10、30、100、300、550或1000 ng PCB 126 kg â1天â1口服,共13周测定大脑组织匀浆中的超氧化物歧化酶(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)的水平。处理导致三种测试酶的活性显着且剂量依赖性地增加。剂量为100-175 mg kg 11 天 ˆ1 时,GSH-Px活性达到最大,而CAT和SOD活性持续增加响应用于本研究的最大剂量。另一方面,GSH水平以剂量依赖性方式被显着抑制。数据表明,先前观察到的大鼠脑组织中PCB-126产生的氧化应激增加与抗氧化剂酶活性和GSH消耗的剂量依赖性增加有关。然而,抗氧化酶活性的增加不能提供完全保护以抵抗由相同剂量引起的氧化损伤。另外,GSH的耗竭在先前观察到的响应于该化合物的氧化应激中起关键作用。

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