Microcystin-LR induces apoptosis in Juvenile Eriocheir sinensis via the mitochondrial pathway
Microcystin-LR (MC-LR), the toxic substance of cyanobacteria secondary metabolism, widely exists in water environments and poses great risks to living organisms. Some toxicological assessments of MC-LR have performed at physiological and biochemical levels. However, plenty of blanks about the potent...
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Veröffentlicht in: | Ecotoxicology and environmental safety 2022-06, Vol.238, p.113528-113528, Article 113528 |
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Zusammenfassung: | Microcystin-LR (MC-LR), the toxic substance of cyanobacteria secondary metabolism, widely exists in water environments and poses great risks to living organisms. Some toxicological assessments of MC-LR have performed at physiological and biochemical levels. However, plenty of blanks about the potential mechanism in aquatic crustacean remains. In this study, we firstly assessed the exposure toxicity of MC-LR to juvenile E. sinensis and clarified that the 96 h LD50 of MC-LR was 73.23 μg/kg. Then, hepatopancreas transcriptome profiles of MC-LR stressed crabs were constructed at 6 h post-injection and 37 differential expressed genes (DEGs) were identified. These DEGs were enriched in cytoskeleton, peroxisome and apoptosis pathways. To further reveal the toxicity of MC-LR, oxidative stress parameters (SOD, CAT, GSH-px and MDA), apoptosis genes (caspase 3, bcl-2 and bax) and apoptotic cells were detected. Significant accumulated MDA and rise-fall enzyme activities verified the oxidative stress caused by MC-LR. It is noteworthy that quantitative real-time PCR and TUNEL assay indicated that MC-LR stress-induced apoptosis via the mitochondrial pathway. Interestingly, activator protein-1 may play a crucial role in mediating the hepatotoxicity of MC-LR by regulating apoptosis and oxidative stress. Taken together, our study investigated the toxic effects and the potential molecular mechanisms of MC-LR on juvenile E. sinensis. It provided useful data for exploring the toxicity of MC-LR to aquatic crustaceans at molecular levels.
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•The 96-h LD50 for MC-LR injected juvenile E. sinensis was 73.23 μg/kg.•MC-LR caused oxidative stress in the hepatopancreas of E. sinensis.•MC-LR induced apoptosis in the hepatopancreas of E. sinensis via the mitochondrial pathway.•MC-LR disturbed the morphology and structure of the hepatopancreas.•AP-1 is involved in apoptosis and redox reactions regulation in the hepatopancreas of E. sinensis. |
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ISSN: | 0147-6513 1090-2414 |
DOI: | 10.1016/j.ecoenv.2022.113528 |