Effects of chronic nitrite exposure on hematological parameters, oxidative stress and apoptosis in spotted seabass (Lateolabrax maculatus) reared at high temperature

亚硝酸盐 丙二醛 高铁血红蛋白 超氧化物歧化酶 氧化应激 血红蛋白 化学 红细胞压积 过氧化氢酶 内分泌学 硫代巴比妥酸 细胞凋亡 TBARS公司 抗氧化剂 乳酸脱氢酶 男科 内科学 生物 生物化学 脂质过氧化 硝酸盐 医学 有机化学
作者
Chen Shen,Shi Cao,Mohamed Mohsen,Xueshan Li,Ling Wang,Kangle Lu,Chunxiao Zhang,Kai Song
出处
期刊:Aquaculture Reports [Elsevier BV]
卷期号:35: 102022-102022 被引量:3
标识
DOI:10.1016/j.aqrep.2024.102022
摘要

The effects of nitrite stress on blood biochemistry, antioxidant capacity, and apoptosis of spotted seabass (Lateolabrax maculatus) under high-temperature conditions were investigated. Fish were subjected to varying levels of nitrite concentrations for 28 days, specifically 0, 8, and 16 mg/L. Blood and gill samples were collected at the 1st, 3rd, 7th, 14th, 21st and 28th of the exposure for index determination, respectively. Results showed that as the concentration of nitrite increased, blood hemoglobin (Hb) and serum chloride ion (Cl-) levels decreased. In addition, compared to the control group, methemoglobin (MetHb), hematocrit (HCT), red blood cells (RBCs), white blood cells (WBCs), and serum potassium ion (K+) were significantly increased in the nitrite-stressed group. In terms of antioxidants, catalase (CAT) and superoxide dismutase (SOD) activities in the gill were significantly decreased with increasing nitrite concentration. Additionally, malondialdehyde (MDA) content was significantly increased with increasing nitrite concentration. Regarding genes related to apoptosis, as nitrite concentration increased, the expressions of hypoxia-inducible factor (Hif-1α) and cytochrome C (Cyt-c) genes in the gill were significantly up-regulated on the 1st and 3rd day of exposure. The expressions of P53, Bax, Caspase-3, Caspase-8, and Caspase-9 genes in the gill were significantly up-regulated in stress groups at different exposure time intervals compared to the control group. In summary, nitrite caused disruption in the balance of blood ions, decreased antioxidant capacity in the gills, increased expression of genes associated with apoptosis, ultimately resulting in gill injury in the spotted seabass.

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