ArticleAnalytical and bioanalytical chemistry2023
Elucidation of the relationship between evodiamine-induced liver injury and CYP3A4-mediated metabolic activation by UPLC-MS/MS analysis.
Article in Analytical and bioanalytical chemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 14 citations in OpenAlex.
- The conversion of evodiamine-induced hepatotoxicity into a therapeutic effect on colonitis: insight from the liver-gut axis mediated by PPAR/NF-κB/ZO-1/caspase-3 pathway.Chinese medicine · 2025Article
- Exploring the biological tissue toxicity and related toxic components of Euodiae Fructus through the multi-tissue spectrum-toxicity relationship.Journal of natural medicines · 2025Article
- Special Issue with Research Topics on "Recent Analysis and Applications of Mass Spectra on Biochemistry".International journal of molecular sciences · 2024Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Evodiamine (EVD), which has been reported to cause liver damage, is the main constituent of Evodia rutaecarpa (Juss.) Benth and may be bioactivated into reactive metabolites mediated by cytochrome P450. However, the relationships between bioactivation and EVD-induced hepatotoxicity remain unknown. In this study, comprehensive hepatotoxicity evaluation was explored, which demonstrated that EVD caused hepatotoxicity in both time- and dose-dependent manners in mice. By application of UPLC-Q/TOF-MS/MS, two GSH conjugates (GM1 and GM2) derived from reactive metabolites of EVD were identified, in microsomal incubation systems exposed to EVD with glutathione (GSH) as trapping agents. CYP3A4 was proved to be the main metabolic enzyme. Correspondingly, the N-acetyl-L-cysteine conjugate derived from the degradation of GM2 was detected in the urine of mice after exposure to EVD. For the first time, the iminoquinone intermediate was found in EVD-pretreated rat bile by the high-resolution MS platform. Pretreatment with ketoconazole protected the animals from hepatotoxicity, decreased the protein expression of cleaved caspase-1 and -3, but increased the area under the serum-concentration-time curve of EVD in blood determined by UPLC-QQQ-MS/MS. Depletion of GSH by buthionine sulfoximine exacerbated EVD-induced hepatotoxicity. These results implicated that the CYP3A4-mediated metabolic activation was responsible for the observed hepatotoxicity induced by EVD.
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