Metabolism of T-2 toxin by blood cell carboxylesterases.
Human and rat blood hydrolysed T-2 toxin along two different pathways giving HT-2 toxin and neosolaniol as primary metabolites, respectively. Neosolaniol represents a metabolic pathway different from that obtained by liver. Rat erythrocytes formed neosolaniol as a primary metabolite whereas white blood cells hydrolysed T-2 toxin to HT-2 toxin. Human erythrocytes formed both HT-2 toxin and neosolaniol whereas all human white cells produced only HT-2 as the primary metabolite. The enzymes responsible for hydrolysis of T-2 toxin to HT-2 toxin in white blood cells and T-2 toxin to neosolaniol in red blood cells were all identified as carboxylesterases by use of specific inhibitors. The ratio between trichothecene hydrolysis and 4-nitrophenyl butyrate hydrolysis varied among the different cell fractions indicating that specific isoenzymes are involved.
Johnsen
H
H
Norwegian Defence Research Establishment, Division for Environmental Toxicology, Kjeller, Norway.
Odden
E
E
Johnsen
B A
BA
Fonnum
F
F
D000818:Animals; D001773:Blood Cells / Q000201:enzymology*; D002265:Carboxylic Ester Hydrolases / Q000097:blood*; D006801:Humans; D006868:Hydrolysis; D051381:Rats; D012717:Sesquiterpenes / Q000097:blood*; D013605:T-2 Toxin / Q000097:blood*
D012717:Sesquiterpenes; D002265:Carboxylic Ester Hydrolases; D013605:T-2 Toxin