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In vitro hepatic aflatoxicol production is related to a higher resistance to aflatoxin B(1) in poultry

A study was conducted to determine the cytosolic in vitro hepatic enzymatic kinetic parameters V(max), K(M), and intrinsic clearance (CL(int)) for aflatoxin B(1) (AFB(1)) reductase [aflatoxicol (AFL) production] and AFL dehydrogenase (AFB(1) production) in four commercial poultry species (chicken, q...

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Detalles Bibliográficos
Autores principales: Murcia, Hansen W., Diaz, Gonzalo J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7099057/
https://www.ncbi.nlm.nih.gov/pubmed/32218462
http://dx.doi.org/10.1038/s41598-020-62415-y
Descripción
Sumario:A study was conducted to determine the cytosolic in vitro hepatic enzymatic kinetic parameters V(max), K(M), and intrinsic clearance (CL(int)) for aflatoxin B(1) (AFB(1)) reductase [aflatoxicol (AFL) production] and AFL dehydrogenase (AFB(1) production) in four commercial poultry species (chicken, quail, turkey and duck). Large differences were found in AFB(1) reductase activity, being the chicken the most efficient producer of AFL (highest CL(int) value). Oxidation of AFL to AFB(1) showed only slight differences among the different poultry species. On average all species produced AFB(1) from AFL at a similar rate, except for the turkey which produced AFB(1) from AFL at a significantly lower rate than chickens and quail, but not ducks. Although the turkey and duck showed differences in AFL oxidation V(max) and K(M) parameters, their CL(int) values did not differ significantly. The ratio AFB(1) reductase/AFL dehydrogenase enzyme activity was inversely related to the known in vivo sensitivity to AFB(1) being highest for the chicken, lowest for the duck and intermediate for turkeys and quail. Since there is no evidence that AFL is a toxic metabolite of AFB(1), these results suggest that AFL production is a detoxication reaction in poultry. Conversion of AFB(1) to AFL prevents the formation of the AFB(1)-8,9-exo-epoxide which, upon conversion to AFB(1)-dihydrodiol, is considered to be the metabolite responsible for the acute toxic effects of AFB(1).