Key Laboratory of Genetic Breeding and Aquaculture Biology of Freshwater Fishes, Ministry of Agriculture, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China.
Wuxi Fisheries College, Nanjing Agricultural University, Wuxi 214081, China; Key Laboratory of Genetic Breeding and Aquaculture Biology of Freshwater Fishes, Ministry of Agriculture, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China.
Fish Shellfish Immunol. 2018 May;76:126-132. doi: 10.1016/j.fsi.2018.02.015. Epub 2018 Feb 10.
Nitrite (NO) can cause oxidative stress in aquatic animal when it accumulates in the organism, resulting in different toxic effects on fish. In the present study, we investigated the effects of nitrite exposure on the antioxidant enzymes and glutathione system in the liver of Bighead carp (Aristichthys nobilis). Fish [Initial average weight: (180.05 ± 0.092) g] were exposed to 48.634 mg/L nitrite for 96 h, and a subsequent 96 h for the recovery test. Fish livers were collected to assay antioxidant enzymes activity, hepatic structure and expression of genes after 0 h, 6 h, 12 h, 24 h, 48 h, 72 h, 96 h of exposure and12 h, 24 h, 48 h, 72 h, 96 h of recovery. The results showed that the activity of glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), and glutathione reductase (GR) increased significantly in the early stages of nitrite exposure. The study also showed that nitrite significantly up-regulated the mRNA levels of glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), and glutathione reductase (GR) after 6, 48, and 72 h of exposure respectively. Nitrite also increased the formation of malondialdehyde (MDA), oxidized glutathione (GSSG), and the activity of catalase (CAT). Nitrite was observed to reduce the activity of superoxide dismutase (SOD) and the level of glutathione (GSH). In the recovery test, GSH and the GSSG recovered but did not return to pre-stress levels. The results suggested that the glutathione system played important roles in nitrite-induced oxidative stress in fish. The bighead carp responds to oxidative stress by enhancing the activity of GSH-Px, GST, GR and up-regulating the expression level of GSH-Px, GST, GR, a whilst simultaneously maintaining the dynamic balance of GSH/GSSG. CAT was also indispensable. They could reduce the degree of lipid peroxidation, and ultimately protect the body from oxidative damage.
亚硝酸盐（NO）在生物体内积累时会导致水生动物产生氧化应激，从而对鱼类产生不同的毒性影响。在本研究中，我们研究了亚硝酸盐暴露对鳙鱼（Aristichthys nobilis）肝脏抗氧化酶和谷胱甘肽系统的影响。将鱼（初始平均体重：（180.05±0.092）g）暴露于 48.634mg/L 亚硝酸盐中 96 小时，随后进行 96 小时恢复试验。在暴露 0、6、12、24、48、72、96 小时以及恢复 12、24、48、72、96 小时后，收集鱼肝以测定抗氧化酶活性、肝结构和基因表达。结果表明，谷胱甘肽过氧化物酶（GSH-Px）、谷胱甘肽 S-转移酶（GST）和谷胱甘肽还原酶（GR）的活性在亚硝酸盐暴露的早期阶段显著增加。研究还表明，亚硝酸盐分别在暴露 6、48 和 72 小时后显著上调了谷胱甘肽过氧化物酶（GSH-Px）、谷胱甘肽 S-转移酶（GST）和谷胱甘肽还原酶（GR）的 mRNA 水平。亚硝酸盐还增加了丙二醛（MDA）、氧化型谷胱甘肽（GSSG）的形成和过氧化氢酶（CAT）的活性。亚硝酸盐还降低了超氧化物歧化酶（SOD）的活性和谷胱甘肽（GSH）的水平。在恢复试验中，GSH 和 GSSG 恢复，但未恢复到应激前水平。结果表明，谷胱甘肽系统在鱼类亚硝酸盐诱导的氧化应激中发挥重要作用。鳙鱼通过增强 GSH-Px、GST、GR 的活性和上调 GSH-Px、GST、GR 的表达水平来应对氧化应激，同时维持 GSH/GSSG 的动态平衡。CAT 也是必不可少的。它们可以降低脂质过氧化的程度，最终保护身体免受氧化损伤。
