Hydroxylation of acetone by ethanol‐ and acetone‐inducible cytochrome P‐450 in liver microsomes and reconstituted membranes

FEBS Letters

Johansson, Inger¹  Eliasson, Erik¹  Ingelman-Sundberg, Magnus¹  Norsten, Carina¹ 

[1] Department of Physiological Chemistry, Karolinska Institute, PO Box 60 400, S-104 01 Stockholm, Sweden

关键词: Acetone;    Cytochrome P-450;    Starvation;    Ketoacidosis;    Gluconeogenesis;    Ethanol;   

DOI  :  10.1016/0014-5793(86)80214-9

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Acetone oxidation in rat liver microsomes was induced 5- or 8-fold by the treatment of the animals with ethanol or acetone, respectively. The apparent K _m of the reaction was 0.9 mM, a value lower than the concentration reported for plasma acetone under starvation conditions. The major acetone metabolite was identified as acetol by GC-MS. Acetone oxidation in microsomes was inhibited by typical P-450 inhibitors as well as by compounds (e.g. imidazole) known to interact with the ethanol-inducible P-450 form. Antibodies against this P-450 isozyme were inhibitory for the reaction in rabbit liver microsomes and this isozyme was the only one that showed acetone hydroxylation activity in reconstituted membranes. Imidazole inhibited the conversion of [¹⁴C]acetone into low-M _r compounds (e.g. glucose) in vivo. It is suggested that the ethanol-and acetone-inducible P-450 make use of acetone as an endogenous substrate in the utilization of the compound for, e.g. glucose production under conditions of starvation and diabetic ketoacidosis.

【 授权许可】

Unknown