Ammonia-induced oxidative stress triggered apoptosis in the razor clam (Sinonovacula constricta)
文献类型: 外文期刊
作者: Guo, Ziqi 1 ; Chen, Yukuan 1 ; Du, Xinxin 1 ; Li, Yifeng 1 ; Niu, Donghong 1 ;
作者机构: 1.Shanghai Ocean Univ, Shanghai Collaborat Innovat Aquat Anim Genet & Bre, Shanghai 201306, Peoples R China
2.Chinese Acad Fishery Sci, Freshwater Fisheries Res Ctr, Key Lab Freshwater Fisheries & Germplasm Resources, Minist Agr & Rural Affairs, Wuxi 214081, Peoples R China
3.Shanghai Ocean Univ, Key Lab Explorat & Utilizat Aquat Genet Resources, Minist Educ, Shanghai 201306, Peoples R China
4.Shanghai Ocean Univ, Coll Fisheries & Life Sci, 999 Hucheng Huan Rd, Shanghai 201306, Peoples R China
关键词: Sinonovacula constricta; Reactive oxygen species; Antioxidant system; Apoptosis; Ammonia
期刊名称:ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH ( 影响因子:5.8; 五年影响因子:5.4 )
ISSN: 0944-1344
年卷期: 2024 年
页码:
收录情况: SCI
摘要: As one of the most significant contaminants and stressors in aquaculture systems, ammonia adversely jeopardizes the health of aquatic animals. Ammonia exposure affects the development, metabolism, and survival of shellfish. However, the responses of the innate immune and antioxidant systems and apoptosis in shellfish under ammonia stress have rarely been reported. In this study, razor clams (Sinonovacula constricta) were exposed to different concentrations of non-ion ammonia (0.25 mg/L, 2.5 mg/L) for 72 h and then placed in ammonia-free seawater for 72 h for recovery. The immune responses induced by ammonia stress on razor clams were investigated by antioxidant enzyme activities and degree of apoptosis in digestive gland and gill tissues at different time points. The results showed that exposure to a high concentration of ammonia greatly disrupted the antioxidant system of the razor clam by exacerbating the accumulation of reactive oxygen species (O-2(-), H2O2) and disordering the activities of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase), and the level of activity remained at a significantly high level after recovering for 72 h (P < 0.05). In addition, there were significant differences (P < 0.05) in the expression of key genes (Caspase 7, Cyt-c, Bcl-2, and Bax) in the mitochondrial apoptotic pathway in the digestive glands and gills of razor clams as a result of ammonia stress and were unable to return to normal levels after 72 h of recovery. TUNEL staining indicated that apoptosis was more pronounced in gills, showing a dose and time-dependent pattern. As to the results, ammonia exposure leads to the activation of innate immunity in razor clams, disrupts the antioxidant system, and activates the mitochondrial pathway of apoptosis. This is important for comprehending the mechanism underlying the aquatic toxicity resulting from ammonia in shellfish.
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