Dichloroacetate (DCA) and trichloroacetate (TCA) were previously found to induce various levels of oxidative stress in the hepatic tissues of mice after subacute and subchronic exposures. The cells are known to have several protective mechanisms against production of oxidative stress by different xenobiotics. To assess the roles of the antioxidant enzymes and glutathione (GSH) in DCA- and TCA-induced oxidative stress, groups of B6C3F1 mice were administered either DCA or TCA at doses of 7.7, 77, 154, and 410 mg kg−1 day−1, by gavage for 4 weeks (4-W) and 13 weeks (13-W), and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as GSH were determined in the hepatic tissues. DCA at doses ranging between 7.7–410, and 7.7–77 mg kg−1 day−1, given for 4-W and 13-W, respectively, resulted in either suppression or no change in SOD, CAT, and GSH-Px activities, but doses of 154–410 mg DCA kg−1 day−1 administered for 13-W were found to result in a significant induction of the three enzyme activities. TCA administration on the other hand, resulted in increases in the SOD and CAT activities, but caused suppression of GSH-Px activity in both the periods. Except for the DCA doses of 77–154 mg kg−1 day−1 administered for 13-W that resulted in a significant reduction in the GSH levels, all other DCA as well as TCA treatments produced no changes in GSH. Since these enzymes are involved in the detoxification of the reactive oxygen species (ROS), superoxide anion (SA), and H2O2, it is concluded that SA is the main contributor to DCA-induced oxidative stress, while both ROS contribute to that of TCA. The increase in the enzyme activities associated with 154–410 mg DCA kg1− day−1 in the 13-W period suggest their role as protective mechanisms contributing to the survival of cells modified in response to those treatments.

中文翻译：

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亚急性和亚慢性暴露后，二氯乙酸盐和三氯乙酸盐对小鼠肝脏中超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性和谷胱甘肽水平的调节

先前发现二氯乙酸盐 (DCA) 和三氯乙酸盐 (TCA) 在亚急性和亚慢性暴露后会在小鼠的肝组织中诱导不同水平的氧化应激。已知这些细胞具有多种保护机制，以防止不同外源性物质产生氧化应激。为了评估抗氧化酶和谷胱甘肽 (GSH) 在 DCA 和 TCA 诱导的氧化应激中的作用，给 B6C3F1 小鼠组施用 DCA 或 TCA，剂量为 7.7、77、154 和 410 mg kg-1 天- 1、通过管饲 4 周 (4-W) 和 13 周 (13-W)，测定超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT) 和谷胱甘肽过氧化物酶 (GSH-Px) 活性，以及​​在肝组织。DCA 的剂量范围为 7.7-410 和 7.7-77 mg kg-1 day-1，分别用于 4-W 和 13-W，导致 SOD、CAT 和 GSH-Px 活性受到抑制或没有变化，但发现 154-410 毫克 DCA kg-1 天-1 的剂量为 13-W 导致三种酶活性的显着诱导. 另一方面，TCA 给药导致 SOD 和 CAT 活性增加，但在这两个时期都抑制了 GSH-Px 活性。除了 77–154 mg kg-1 day-1 的 DCA 剂量 13-W 导致 GSH 水平显着降低外，所有其他 DCA 和 TCA 治疗均未产生 GSH 变化。由于这些酶参与活性氧 (ROS)、超氧阴离子 (SA) 和 H2O2 的解毒，因此可以得出结论，SA 是 DCA 诱导的氧化应激的主要贡献者，而两种 ROS 都有助于 TCA 的解毒.