Publications
Detailed Information
Lipid metabolism, immune and apoptosis transcriptomic responses of the hepatopancreas of Chinese mitten crab to the exposure to microcystin-LR
Cited 6 time in
Web of Science
Cited 6 time in Scopus
- Authors
- Issue Date
- 2022-05
- Publisher
- Academic Press
- Citation
- Ecotoxicology and Environmental Safety, Vol.236, p. 113439
- Abstract
- © 2022 The AuthorsGlobal warming is favouring the incidence, intensity and duration of harmful cyanobacterial blooms. Microcystin-LR (MC-LR), a hepatotoxic agent, is produced during cyanobacterial blooms. To understand the molecular mechanisms of acute hepatotoxic effect of low doses of MC-LR in crab, we examined differentially expressed genes in samples of the hepatopancreas of Chinese mitten crab (Eriocheir sinensis) collected in 48 h after injections of MC-LR at doses of 0, 25, 50, and 75 µg/kg. The results revealed that MC-LR induced changes in corresponding gene led to the accumulation of triglycerides. MC-LR exposure affected sterol metabolism. Apoptosis-related genes such as Fas-L, Bcl-XL, Cytc, AiF, p53, PERK, calpain, CASP2, CASP7, α-tubulin, PARP, GF, G12, and PKC were upregulated. Conversely, expression levels of CASP10 and ASK1 were downregulated. Genes related to the regulation of actin cytoskeleton (Rho, ROCK, MLCP, MLC, PAK, and PFN) were upregulated. Further, expression levels of genes encoding fatty acid elongation-related enzymes were upregulated, but the expression of genes related to fatty acid synthesis was slightly down regulated. Taken together, these results demonstrated the hepatic toxicity and molecular mechanisms of changes in lipid metabolism, immune and apoptosis in Chinese mitten crab under the MC-LR-induced stress, which is the first report on crabs and performs a comprehensive analysis and a new insight of the molecular toxicological responses in crabs.
- ISSN
- 0147-6513
- Files in This Item:
- There are no files associated with this item.
- Appears in Collections:
Item View & Download Count
Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.