Abstract Hypoxia induces cell death through excessive production of reactive oxygen species (ROS) and calcium (Ca2+) influx in cells and TRPM2 cation channel is activated by oxidative stress. Zinc (Zn), selenium (Se), and glutathione (GSH) have antioxidant properties in several cells and hypoxia-induced TRPM2 channel activity, ROS and cell death may be inhibited by the Zn, Se, and GSH treatments. We investigated effects of Zn, Se, and GSH on lipid peroxidation (LPO), cell cytotoxicity and death through inhibition of TRPM2 channel activity in transfected HEK293 cells exposed to hypoxia defined as oxygen deficiency. We induced four groups as normoxia 30 and 60 min evaluated as control groups, hypoxia 30 and 60 min in the HEK293 cells. The cells were separately pre-incubated with extracellular Zn (100 µM), Se (150 nM) and GSH (5 mM). Cytotoxicity was evaluated by lactate dehydrogenase (LDH) release and the LDH and LPO levels were significantly higher in the hypoxia-30 and 60 min-exposed cells according to normoxia 30 and 60 min groups. Furthermore, we found that the LPO and LDH were decreased in the hypoxia-exposed cells after being treated with Zn, Se, and GSH according to the hypoxia groups. Compared to the normoxia groups, the current densities of TRPM2 channel were increased in the hypoxia-exposed cells by the hypoxia applications, while the same values were decreased in the treatment of Zn, Se, and GSH according to hypoxia group. In conclusion, hypoxia-induced TRPM2 channel activity, ROS and cell death were recovered by the Se, Zn and GSH treatments.

中文翻译：

---

锌、硒和谷胱甘肽对转染 HEK293 细胞缺氧诱导的 TRPM2 通道激活的潜在保护作用

摘要 缺氧通过细胞内活性氧 (ROS) 和钙 (Ca2+) 的过量产生诱导细胞死亡，TRPM2 阳离子通道被氧化应激激活。锌 (Zn)、硒 (Se) 和谷胱甘肽 (GSH) 在几种细胞中具有抗氧化特性，缺氧诱导的 TRPM2 通道活性、ROS 和细胞死亡可能会受到 Zn、Se 和 GSH 处理的抑制。我们通过抑制暴露于缺氧定义的缺氧的转染 HEK293 细胞中的 TRPM2 通道活性，研究了 Zn、Se 和 GSH 对脂质过氧化 (LPO)、细胞毒性和死亡的影响。我们在 HEK293 细胞中诱导四组作为正常氧 30 和 60 分钟评估为对照组，缺氧 30 和 60 分钟。细胞分别与细胞外 Zn (100 µM)、Se (150 nM) 和 GSH (5 mM) 预孵育。通过乳酸脱氢酶 (LDH) 释放评估细胞毒性，根据常氧 30 和 60 分钟组，低氧 30 和 60 分钟暴露细胞中的 LDH 和 LPO 水平显着更高。此外，我们发现根据缺氧组用锌、硒和谷胱甘肽处理后，缺氧暴露细胞中的 LPO 和 LDH 降低。与常氧组相比，缺氧组的TRPM2通道电流密度增加，而缺氧组在Zn、Se和GSH处理中均降低。总之，硒、锌和谷胱甘肽处理可恢复缺氧诱导的 TRPM2 通道活性、活性氧和细胞死亡。