当前位置: X-MOL 学术Ital. J. Anim. Sci. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Effects of ammonia-N stress on the antioxidant enzymes, heat shock proteins, and apoptosis-related genes of Macrobrachium rosenbergii
Italian Journal of Animal Science ( IF 2.5 ) Pub Date : 2021-03-04 , DOI: 10.1080/1828051x.2021.1886612
Xuexing Dong 1 , Qigen Liu 2 , Weihong Zhao 1 , Jiangtao Ou 1 , FengJuan Jiang 1 , Haisong Guo 1 , Linlan Lv 1
Affiliation  

Abstract

Current study explored the acute toxicity and oxidative stress of ammonia-N on Macrobrachium rosenbergii. Prawns were exposed to ammonia-N at 3.01, 3.55, 4.18, 4.92, 5.80, 6.82, and 8.04 mg·L−1 for a 96 h acute toxicity test. In the subsequent sublethal toxicity text, they were exposed to ammonia-N at 0.5 or 1.88 mg·L−1 (1/2 96 h LC50) for 3, 8, 12, 24, 48, and 72 h. The total superoxide dismutase (T-SOD) activity, catalase (CAT) activity and malondialdehyde (MDA) content were detected in the muscle, haemolymph, and gill. The gene expression of antioxidases (Cu/ZnSOD, CAT, GPX), heat shock proteins (HSP60, HSP70, HSP90), and apoptosis-related genes (Caspase 3, Bok) in the muscle and hepatopancreas also was evaluated. The LC50 values of non-ionic ammonia at 24, 48, 72, and 96 h were 7.72, 5.44, 4.28, and 3.78 mg·L−1, respectively. Ammonia-N significantly affected the T-SOD and CAT activities in the haemolymph and gill but not in the muscle. After 72 h of ammonia-N exposure, MDA content in the muscle, haemolymph, and gill in 1.88 mg·L−1 group significantly increased. The relative mRNA expression of antioxidant enzymes, heat shock proteins and Caspase 3 were upregulated in the hepatopancreas and muscle after ammonia exposure, especially in 1.88 mg·L−1. This result suggested that 1/2 96 h LC50 ammonia exposure induced severe oxidative stress, eventually even apoptosis of M. rosenbergii through the caspase pathway.

  • Highlights
  • Half of 96 h LC50 ammonia-N caused severe oxidative stress on M. rosenbergii.

  • Ammonia-N induced the antioxidase and HSP to protect cells from oxidative stress.

  • Ammonia-N induced mRNA expression level of Caspase 3 of M. rosenbergii.



中文翻译:

氨氮胁迫对罗氏沼虾抗氧化酶,热休克蛋白和凋亡相关基因的影响

摘要

目前的研究探索了氨氮对罗氏沼虾的急性毒性和氧化应激将虾暴露于3.01、3.55、4.18、4.92、5.80、6.82和8.04 mg·L -1的氨氮下,进行96小时急性毒性试验。在随后的亚致死毒性文本中,将它们暴露于0.5或1.88 mg·L -1(1/2 96 h LC50)的氨氮中3、8、12、24、48和72 h。在肌肉,血淋巴和g中检测到总超氧化物歧化酶(T-SOD)活性,过氧化氢酶(CAT)活性和丙二醛(MDA)含量。抗氧化酶(Cu / ZnSODCATGPX),热休克蛋白(HSP60HSP70HSP90)的基因表达。),并评估了肌肉和肝胰腺中与凋亡相关的基因(Caspase 3Bok)。非离子氨在24、48、72和96 h的LC50值分别为7.72、5.44、4.28和3.78 mg·L -1。氨氮显着影响血淋巴和腮中的T-SOD和CAT活性,但不影响肌肉中的T-SOD和CAT活性。氨氮暴露72 h后,1.88 mg·L -1组的肌肉,血淋巴和g中MDA含量显着增加。氨暴露后,肝胰腺和肌肉中抗氧化酶,热休克蛋白和Caspase 3的相对mRNA表达上调,尤其是在1.88 mg·L -1时。该结果表明1/2 96 h LC50氨暴露引起严重的氧化应激,甚至通过半胱天冬酶途径甚至导致罗氏沼虾的细胞凋亡。

  • 强调
  • 96小时LC50氨氮中的一半在罗氏沼虾上引起了严重的氧化应激

  • 氨氮诱导抗氧化酶和HSP保护细胞免受氧化应激。

  • 氨-N诱导的mRNA表达水平胱天蛋白酶3罗氏沼虾

更新日期:2021-03-04
down
wechat
bug