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•Rhizoma Paridis exposure treatment caused an obvious toxic effect on the zebrafish liver, resulting in a significant change of the liver organization structure and various biochemical parameters.•The hepatotoxicity of adult zebrafish liver induced by Rhizoma Paridis was mainly associated with lipid metabolism and energy metabolism disorder. Oxidative stress injury, inflammation, and endoplasmic reticulum stress might also be involved in the hepatotoxicity of Rhizoma Paridis.•The metabolomics based on GC-MS and iTRAQ quantitative proteomics analyses were performed to analyze the metabolites and protein profile changes of liver tissues of adult zebrafish. And the result showed that mitochondria was the main toxic target for Rhizoma Paridis-induced hepatotoxicity.
Rhizoma Paridis hepatotoxicity is a risk factor limiting its extensive use in clinic, there is limited information available regarding the mechanism by which typical environmental levels of exposure can contribute to the onset of this disease. The adult zebrafish were exposed to Rhizoma Paridis at a sub-lethal concentration. The alterations in protein expression profiles and metabolite levels in the adult zebrafish liver, a popular model for toxicity assessment, exposed to the Rhizoma Paridis were observed. The result showed that Rhizoma Paridis exposure treatment caused an obvious toxic effect on the zebrafish liver, resulting in a significant change of the liver organization structure and various biochemical parameters. The hepatotoxicity of adult zebrafish liver induced by Rhizoma Paridis was mainly associated with lipid metabolism and energy metabolism disorder. Furthermore, oxidative stress injury, inflammation, and endoplasmic reticulum stress might also be involved in the hepatotoxicity. Our study facilitated the understanding of molecular signatures of toxic effects of Rhizoma Paridis causing liver injury to move away from the risk assessment based on in vivo animal experiments.