Untersuchungen zum Einfluß von Ascorbinsäure und Dehydroascorbinsäure auf die Hydroxylierung von Acetanilid mit Lebermikrosomen von Ratten

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Abstract
In vitro studies on the hydroxylation of acetanilide with liver microsomes from benzpyrene-treated rats with reduced nicotinamide adenine dinucleotide-phosphate as the electron donor showed the following: In about 50% of the experiments, ascorbic acid is inhibitory; occasionally it activates and otherwise has no effect on the microsomal p-hydroxylation. De-hydroascorbic acid causes an average increase of about 20% in the enzymatic p-hydroxylation. Preincubation of the microsomes at pH 8 causes a loss of ascorbic acid and a corresponding decrease in the p-hydroxylation activity. Addition of ascorbic acid or dehydroascorbic acid almost completely restores the hydroxylation activity. The un-physiological single electron carrier, dihydroxyfumarate, can replace dehydroascorbic acid or ascorbic acid in the in vitro experiment. Ascorbic acid appears to be a physiological but non-specific activator of microsomal hydroxylation.