College of Fisheries, Huazhong Agricultural University, Wuhan, 430070, China.
Engineering Research Center of Green Development for Conventional Aquatic Biological Industry in the Yangtze River Economic Belt, Ministry of Education, Wuhan, 430070, China.
Biol Trace Elem Res. 2022 Aug;200(8):3876-3884. doi: 10.1007/s12011-021-02982-x. Epub 2021 Nov 2.
The present study was conducted to investigate the protective effects of selenium on the oxidative damage of kidney cells (CIK) caused by nitrite exposure in grass carp (Ctenopharyngodon idella). Cells were pre-incubated by NaSeO (10 μmol/L) for 12 h and then exposed to NaNO (25 mg/L) for 24 h, the cell viability, apoptosis, gene expression, and antioxidant enzyme activity were assayed. The results show that nitrite reduced cell viability and induced apoptosis, and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) as well as the sod, cat, and gpx genes reduced (p < 0.05), while the intracellular calcium ion concentration increased (p < 0.05). Interestingly, selenium treatment significantly alleviated the nitrite induced changes in cell growth, apoptosis, and calcium influx. The cell viability after low-concentration selenium treatment is higher than that of normal cells (p < 0.05). CIK cells were pre-incubated with NaSeO and then exposed to NaNO, the antioxidant indicators could be maintained at normal levels. And compared with nitrite exposure, intracellular calcium ion concentration and apoptotic rate of selenium-incubated still decreased. The expressions of Nrf2 and Keap1 genes increased significantly in CIK cells treated with sodium selenite for 12 h, and the same trend as the enzyme activities of this group. The results show that the supplement of selenium can enhance the cell's resistance to sodium nitrite exposure to a certain extent, by alleviating the antioxidant imbalance, high apoptosis rate, and intracellular calcium ion disturbance caused by nitrite exposure. And the Nrf2-Keap1 pathway may play an important role in the process.
本研究旨在探讨亚硒酸钠对亚硝酸钠暴露引起草鱼肾细胞（CIK）氧化损伤的保护作用。细胞用 NaSeO（10 μmol/L）预孵育 12 h 后，再用 NaNO（25 mg/L）处理 24 h，检测细胞活力、凋亡、基因表达和抗氧化酶活性。结果表明，亚硝酸钠降低了细胞活力并诱导了细胞凋亡，超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）的活性以及 sod、cat 和 gpx 基因的表达均降低（p < 0.05），而细胞内钙离子浓度增加（p < 0.05）。有趣的是，硒处理显著缓解了亚硝酸钠引起的细胞生长、凋亡和钙离子内流的变化。低浓度硒处理后的细胞活力高于正常细胞（p < 0.05）。CIK 细胞用 NaSeO 预孵育后再用 NaNO 处理，抗氧化指标可维持在正常水平。与亚硝酸钠暴露相比，硒孵育后的细胞内钙离子浓度和凋亡率仍有所降低。用亚硒酸钠处理 12 h 的 CIK 细胞中 Nrf2 和 Keap1 基因的表达明显增加，与该组的酶活性呈相同趋势。结果表明，硒的补充可以在一定程度上增强细胞对亚硝酸钠暴露的抵抗力，缓解亚硝酸钠暴露引起的抗氧化失衡、高凋亡率和细胞内钙离子紊乱。Nrf2-Keap1 通路可能在这一过程中发挥重要作用。
