Mechanisms of ammonotelism, epithelium damage, cellular apoptosis, and proliferation in gill of Litopenaeus vannamei under NH 4 Cl exposure.

Autor: Li Y; The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao, 266003, People's Republic of China., Zhang X; The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao, 266003, People's Republic of China., Tong R; The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao, 266003, People's Republic of China., Xu Q; The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao, 266003, People's Republic of China., Zhang N; The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao, 266003, People's Republic of China., Liao Q; The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao, 266003, People's Republic of China., Pan L; The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao, 266003, People's Republic of China. panlq@ouc.edu.cn.
Jazyk: angličtina
Zdroj: Environmental science and pollution research international [Environ Sci Pollut Res Int] 2024 Feb; Vol. 31 (10), pp. 15153-15171. Date of Electronic Publication: 2024 Jan 30.
DOI: 10.1007/s11356-024-32111-9
Abstrakt: Excessive ammonia-N in coastal environment and aquaculture threatens the health of marine organisms. To explore the mechanism of gill damage induced by ammonia-N, transcriptome of Litopenaeus vannamei 's gill was carried out under 20 mg/L NH 4 Cl for 0, 6, and 48 h. K-means clustering analysis suggested that ammonia excretion and metabolism-related genes were elevated. GO and KEGG enrichment analysis suggested that glycosyltransferase activity and amino acid metabolism were affected by ammonia. Moreover, histological observation via three staining methods gave clues on the changes of gill after ammonia-N exposure. Increased mucus, hemocyte infiltration, and lifting of the lamellar epithelium suggested that gill epithelium was suffering damage under ammonia-N stress. Meanwhile, the composition of extracellular matrix (ECM) in connective tissue changed. Based on the findings of transcriptomic and histological analysis, we further investigated the molecular mechanism of gill damage under multiple concentrations of NH 4 Cl (0, 2, 10, 20 mg/L) for multiple timepoints (0, 3, 6, 12, 24, 48, 72 h). First, ammonia excretion was elevated via ion channel, transporter, and exocytosis pathways, but hemolymph ammonia still kept at a high level under 20 mg/L NH 4 Cl exposure. Second, we focused on glycosaminoglycan metabolism which was related to the dynamics of ECM. It turned out that the degradation and biosynthesis of chondroitin sulfate (CS) were elevated, suggesting that the structure of CS might be destructed under ammonia-N stress and CS played an important role in maintaining gill structure. It was enlightening that the destructions occurred in extracellular regions were vital to gill damage. Third, ammonia-N stress induced a series of cellular responses including enhanced apoptosis, active inflammation, and inhibited proliferation which were closely linked and jointly led to the impairment of gill. Our results provided some insights into the physiological changes induced by ammonia-N and enriched the understandings of gill damage under environmental stress.
(© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
Databáze: MEDLINE
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