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.

中文翻译：

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

在亚慢性暴露后，检测了不同剂量的 3,3',4,4',5-五氯联苯 (PCB126) 诱导大鼠脑组织抗氧化酶活性和谷胱甘肽水平变化的能力。给各组大鼠施用 10、30、100、300、550 或 1000 ng PCB 126 kg−1 day−1，po，持续 13 周，并观察超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT) 和谷胱甘肽过氧化物酶的活性(GSH-Px) 以及脑组织匀浆中的谷胱甘肽 (GSH) 水平。治疗导致三种测试酶的活性显着且剂量依赖性增加。虽然在 100–175 mg kg-1 day-1 的剂量下实现了 GSH-Px 活性的最大增加，但响应于本研究使用的最大剂量，CAT 和 SOD 活性继续增加。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 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并不能提供针对相同剂量诱导的氧化损伤的完全保护。此外，谷胱甘肽耗竭在先前观察到的氧化应激反应中起着关键作用。抗氧化酶活性的增加不能提供完全保护以防止相同剂量引起的氧化损伤。此外，谷胱甘肽耗竭在先前观察到的氧化应激反应中起着关键作用。抗氧化酶活性的增加不能提供完全保护以防止相同剂量引起的氧化损伤。此外，谷胱甘肽耗竭在先前观察到的氧化应激反应中起着关键作用。