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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Concerted action of sulfiredoxin and peroxiredoxin I protects against alcohol-induced oxidative injury in mouse liver.
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Concerted action of sulfiredoxin and peroxiredoxin I protects against alcohol-induced oxidative injury in mouse liver.

机译：磺胺类毒素和过氧化物类毒素I的协同作用可防止酒精引起的小鼠肝脏氧化损伤。

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摘要

Peroxiredoxins (Prxs) are peroxidases that catalyze the reduction of reactive oxygen species (ROS). The active site cysteine residue of members of the 2-Cys Prx subgroup (Prx I to IV) of Prxs is hyperoxidized to cysteine sulfinic acid (Cys-SO(2) ) during catalysis with concomitant loss of peroxidase activity. Reactivation of the hyperoxidized Prx is catalyzed by sulfiredoxin (Srx). Ethanol consumption induces the accumulation of cytochrome P450 2E1 (CYP2E1), a major contributor to ethanol-induced ROS production in the liver. We now show that chronic ethanol feeding markedly increased the expression of Srx in the liver of mice in a largely Nrf2-dependent manner. Among Prx I to IV, only Prx I was found to be hyperoxidized in the liver of ethanol-fed wildtype mice, and the level of Prx I-SO(2) increased to approximately 30% to 50% of total Prx I in the liver of ethanol-fed Srx(-/-) mice. This result suggests that Prx I is the most active 2-Cys Prx in elimination of ROS from the liver of ethanol-fed mice and that, despite the up-regulation of Srx expression by ethanol, the capacity of Srx is not sufficient to counteract the hyperoxidation of Prx I that occurs during ROS reduction. A protease protection assay revealed that a large fraction of Prx I is located together with CYP2E1 at the cytosolic side of the endoplasmic reticulum membrane. The selective role of Prx I in ROS removal is thus likely attributable to the proximity of Prx I and CYP2E1. CONCLUSION: The pivotal functions of Srx and Prx I in protection of the liver in ethanol-fed mice was evident from the severe oxidative damage observed in mice lacking either Srx or Prx I.
机译：过氧化物酶（Prxs）是过氧化物酶，可催化还原活性氧（ROS）。 Prxs的2-Cys Prx子组成员（Prx I至IV）的活性位点半胱氨酸残基在催化过程中被过氧化为半胱氨酸亚磺酸（Cys-SO（2）），并伴有过氧化物酶活性的损失。过氧化的Prx的再活化是由磺基还原毒素（Srx）催化的。乙醇的摄入会诱导细胞色素P450 2E1（CYP2E1）的积累，而细胞色素P450 2E1（CYP2E1）是乙醇诱导肝脏中ROS产生的主要因素。我们现在显示，慢性乙醇喂养以很大程度上依赖Nrf2的方式显着增加了小鼠肝脏Srx的表达。在Prx I至IV中，仅以乙醇喂养的野生型小鼠肝脏中的Prx I被过氧化，并且Prx I-SO（2）的水平增加到肝脏中总Prx I的30％至50％乙醇喂养的Srx（-/-）小鼠。该结果表明，Prx I是在乙醇喂养的小鼠肝脏中清除ROS的最活跃的2-Cys Prx，尽管乙醇对Srx表达的上调作用，但Srx的能力不足以抵消这种作用。 ROS还原过程中发生的Prx I过度氧化。蛋白酶保护试验表明，大部分Prx I与CYP2E1一起位于内质网膜的胞质侧。因此，Prx I在ROS去除中的选择性作用可能归因于Prx I和CYP2E1的接近。结论：从缺乏Srx或Prx I的小鼠中观察到严重的氧化损伤，可以明显看出Srx和Prx I在保护乙醇喂养的小鼠肝脏中的关键功能。

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