ArticleEuropean journal of drug metabolism and pharmacokinetics2017
Hydroxylation Metabolisms of Crassicauline A in Rats Under Toxic Dose.
Article in European journal of drug metabolism and pharmacokinetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed, 10 citations in OpenAlex.
- Aconitine and its derivatives: bioactivities, structure-activity relationships and preliminary molecular mechanisms.Frontiers in chemistry · 2024Review
- Classification, Toxicity and Bioactivity of Natural Diterpenoid Alkaloids.Molecules (Basel, Switzerland) · 2021Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
objectivesCrassicauline A, a C
methodsUsing a de novo developed and validated UPLC-MS/MS method, excretion studies in rats were carried out to investigate the recoveries of crassicauline A and its hydroxylated metabolites in urine and feces. Mass fragmentation analysis was used to identify the detected hydroxylated metabolites. In vitro metabolism assay in liver S9 fraction was employed to preliminarily investigate the inter-species difference of hydroxylation metabolism between rats and human.
resultsAt a toxic dose of 100 µg/kg, less than 10% and 5% of the administrated dose of crassicauline A were recovered in the urine and feces after single intravenous and oral administration, respectively. Trace of yunaconitine, a possible 3-hydroxylated metabolite of crassicauline A, was detected in urine samples, but not considered to be derived from the in vivo metabolism, because the recovered yunaconitine and crassicauline A was equivalent to their occurrences in the test article. Another hydroxylated metabolite was detected with much higher levels than yunaconitine. Based on chromatographic behaviors and fragmentation analysis, the hydroxylation site of this metabolite was tentatively identified at C-15 on the skeleton, which might have produced a toxic alkaloid known as deoxyjesaconitine. The in vivo observations were consistent with the preliminary in vitro results in liver S9 fraction, in which an inter-species difference was highlighted that rats demonstrated more hydroxylation than human did.
conclusionsThis work disclosed that crassicauline A is elimilated in rats predominantly by metabolism under toxic dosage and the hydroxylation probably at C-15 might be a potential bioactivation pathway in both rats and human.
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