Microcystin-LR induces histopathological injury and cell apoptosis in the hepatopancreas of white shrimp, Litopenaeus vannamei.

Ecotoxicol Environ Saf

State Key Laboratory of Mariculture Biobreeding and Sustainable Goods, Yellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Qingdao, Shandong 266071, China; Laboratory for Marine Fisheries Science and Food Production Processes, Qingdao Marine Science and Technology Center, Qingdao, Shandong 266237, China. Electronic address:

Published: October 2024

Microcystin-LR (MC-LR), a common hepatotoxin produced by bloom-forming cyanobacteria, presents a serious threat to the health of aquatic animals. In this study, we studied the impact of MC-LR on hepatopancreas histopathology, enzyme activity, transcriptome, and apoptosis of Litopenaeus vannamei. Thus, shrimp postlarvae (1.63 ± 0.5 g) exposed to MC-LR at 500 μg/kg caused morphological lesions in the histology of the shrimp hepatopancreas, which exhibited swollen, lighter coloration and unclear edges. Moreover, MC-LR significantly altered the hepatopancreas enzyme activities such as the levels of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), acid phosphatase (ACP), alkaline phosphatase (AKP) and lysozyme (LZM), including the state of apoptosis in hepatopancreas. From the RNA-seq analysis of the hepatopancreas, a total of 728 differentially expressed genes (DEGs) were identified, and their functions in MC-LR treatment group were involved in cellular processes, metabolic processes, biological regulation, cellular components, catalytic activity and binding. The metabolic pathways primarily associated with the DEGs included reactive oxygen species, glycerophospholipid metabolism and the phospholipase D signaling pathway. Overall, q-PCR results indicated that MC-LR led to significant changes in multiple apoptosis genes of shrimp hepatopancreas. This study expand the understanding of the effect of microcystin-LR on commercially farmed crustaceans.

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http://dx.doi.org/10.1016/j.ecoenv.2024.117059DOI Listing

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