Dioxin-elicited decrease in cobalamin redirects hepatic propionyl-CoA metabolism to the β-oxidation-like pathway resulting in acrylyl-CoA conjugate accumulation
K. Orlowska, R. R. Fling, R. Nault, W. J. Sink, A. L. Schilmiller, T. Zacharewski
This study shows TCDD decreases cobalamin, inhibits MUT activity, and redirects propionyl-CoA metabolism to a Cbl-independent β-oxidation-like pathway, leading to acrylyl-CoA accumulation and hepatotoxicity.
bioRxiv · Mar 24, 2021Pharmacology & Toxicology