Fisheries College of Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Animal Disease Control and Healthy culture & Key Laboratory of Control for Disease of Aquatic Animals of Guangdong Higher Education Institutes, Zhanjiang, 524088, China.
Fisheries College of Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Animal Disease Control and Healthy culture & Key Laboratory of Control for Disease of Aquatic Animals of Guangdong Higher Education Institutes, Zhanjiang, 524088, China.
Fish Shellfish Immunol. 2022 Nov;130:72-78. doi: 10.1016/j.fsi.2022.08.069. Epub 2022 Sep 8.
Oxidative stress caused by ammonia and nitrite, affect the health and growth of aquaculture animals, results in oxidative damages. However, the toxic mechanism and pathogenesis of ammonia and nitrite to aquatic invertebrates are not completely clear. The present study was conducted to investigate the effects of sub-lethal ammonia and nitrite on autophagy and apoptosis in hepatopancreas of Pacific whiteleg shrimp Litopenaeus vannamei. Shrimps were exposed to sub-lethal ammonia (20 mg/L) and nitrite (20 mg/L) for 72 h, respectively. Hepatopancreas was collected for investigating the autophagy and apoptosis under stress conditions. The results showed that ammonia stress could induce up-regulated of autophagy (ATG3, ATG4, ATG10 and ATG12) and apoptosis (Caspase3 and P53) genes transcription. Nitrite stress could also induce up-regulated of autophagy (ATG3, ATG4, ATG5 and ATG10) and apoptosis (Caspase3) genes transcription. The expression of the autophagy related genes increased at first and then decreased with increasing exposure time. The atrophy, lysis, vacuolation of cell and other tissue damages in hepatopancreas were observed after 72h exposure to ammonia and nitrite. The results indicated that ammonia and nitrite stress could induce autophagy and apoptosis, and results in oxidative damage.
氨氮和亚硝酸盐引起的氧化应激会影响水产养殖动物的健康和生长,导致氧化损伤。然而,氨氮和亚硝酸盐对水生无脊椎动物的毒性机制和发病机制尚不完全清楚。本研究旨在探讨亚致死浓度的氨氮和亚硝酸盐对凡纳滨对虾(Litopenaeus vannamei)肝胰腺自噬和细胞凋亡的影响。将虾分别暴露于亚致死浓度的氨氮(20mg/L)和亚硝酸盐(20mg/L)中 72h,收集肝胰腺,研究应激条件下的自噬和凋亡情况。结果表明,氨氮胁迫可诱导自噬(ATG3、ATG4、ATG10 和 ATG12)和凋亡(Caspase3 和 P53)基因转录的上调。亚硝酸盐胁迫也能诱导自噬(ATG3、ATG4、ATG5 和 ATG10)和凋亡(Caspase3)基因转录的上调。自噬相关基因的表达先增加后减少,随着暴露时间的增加而减少。氨氮和亚硝酸盐暴露 72h 后,肝胰腺出现细胞萎缩、溶解、空泡化和其他组织损伤。结果表明,氨氮和亚硝酸盐胁迫可诱导自噬和细胞凋亡,导致氧化损伤。