Red blood cell death or erythrocyte apoptosis (eryptosis) is generally mediated by oxidative stress, energy depletion, heavy metals exposure, or xenobiotics. As erythrocytes are a major target for oxidative stress due to their primary function as O₂-carrying cells, they possess an efficient antioxidant defense system consisting of glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), and peroxiredoxin 2 (Prx2). The oxidative stress-mediated activation of the Ca²⁺-permeable cation channel results in Ca²⁺ entry into the cells and subsequent cell death. Herein, we describe for the first time that selenium compounds having intramolecular diselenide or selenenyl sulfide moieties can prevent the oxidative stress-induced eryptosis by exhibiting an unusual Prx2-like redox activity under conditions when the cellular Prx2 and CAT enzymes are inhibited.

中文翻译：

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Peroxiredoxin模拟物对红细胞中氧化还原信号和硫醇稳态的调节。

红细胞死亡或红细胞凋亡（加密）通常是由氧化应激，能量消耗，重金属暴露或异种生物介导的。由于红细胞由于其主要功能为携带O _2的细胞而成为氧化应激的主要靶标，因此它们具有由谷胱甘肽过氧化物酶（GPx），超氧化物歧化酶（SOD），过氧化氢酶（CAT）和过氧化物酶2组成的有效抗氧化防御系统。 （Prx2）。Ca ²⁺渗透性阳离子通道的氧化应激介导的活化导致Ca ²⁺进入细胞并随后死亡。在本文中，我们首次描述了具有分子内二硒化物或硒烯基硫化物部分的硒化合物可在抑制细胞Prx2和CAT酶的条件下表现出异常的Prx2样氧化还原活性，从而防止氧化应激诱导的加密。