South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou, PR China.
Key Laboratory of South China Sea Fishery Resources Exploitation & Utilization, Ministry of Agriculture, Guangzhou, PR China.
J Exp Zool A Ecol Integr Physiol. 2018 Jan;329(1):43-50. doi: 10.1002/jez.2162. Epub 2018 Apr 20.
The acute toxicity of nitrite on the mucosal morphology and oxidative stress response was investigated in the intestines of Litopenaeus vannamei after the exposure of 20 mg/L nitrite for 72 hr. The duration of nitrite stress influenced the shrimp survival, and the cumulative mortality rate was 36.7% at 72 hr. Hematoxylin and eosin (HE) stain showed that nitrite stress damaged the intestine connective and epithelium tissue. Specifically, nitrite stress increased the content of reactive oxygen species (ROS) production (O generation capacity), lipid peroxidation (LPO), and malondialdehyde (MDA). Meanwhile, the activities of antioxidant enzymes including superoxide dismutase (SOD) increased first, then catalase (CAT) and glutathione peroxidase (GPx) increased to the highest at 24 and 12 hr, respectively. The relative expression level of antioxidant genes including heat shock protein 70 (HSP70), ferritin, and thioredoxin (Trx) increased to the highest at 6, 12, and 48 hr respectively. After exposure to nitrite stress for 72 hr, the levels of antioxidant enzymes activity and genes expression all decreased. These results revealed that nitrite stress harmed the intestine barrier of L. vannamei by damaging the mucosal structure, inducing the oxidative stress, and confusing the antioxidant status.
研究了 20mg/L 亚硝酸盐暴露 72 小时后凡纳滨对虾肠道中亚硝酸盐对黏膜形态和氧化应激反应的急性毒性。亚硝酸盐应激持续时间影响虾的存活率,72 小时时累积死亡率为 36.7%。苏木精-伊红(HE)染色显示,亚硝酸盐应激破坏了肠连接组织和上皮组织。具体来说,亚硝酸盐应激增加了活性氧(ROS)产生(O 生成能力)、脂质过氧化(LPO)和丙二醛(MDA)的含量。同时,抗氧化酶活性如超氧化物歧化酶(SOD)先增加,然后过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)分别在 24 和 12 小时增加到最高。抗氧化基因如热休克蛋白 70(HSP70)、铁蛋白和硫氧还蛋白(Trx)的相对表达水平分别在 6、12 和 48 小时增加到最高。暴露于亚硝酸盐应激 72 小时后,抗氧化酶活性和基因表达水平均下降。这些结果表明,亚硝酸盐应激通过破坏黏膜结构、诱导氧化应激和扰乱抗氧化状态来损害凡纳滨对虾的肠道屏障。