Abstract
The role of aromatic hydrocarbon receptor (AhR)-mediated signal transduction pathways was investigated in the regulation of ascorbate synthesis by using Ah-responsive and Ah-unresponsive mouse strains. In vivo 3-methylcholanthrene treatment increased hepatic and plasma ascorbate concentrations only in the Ah-responsive strain. The mRNA level of gulonolactone oxidase and the microsomal ascorbate production from p-nitrophenyl glucuronide, D-glucuronic acid or gulonolactone in the liver of Ah-responsive and Ah-unresponsive mice were compared. In Ah-responsive mice, these parameters were higher originally, and they further increased upon in vivo addition of 3-methylcholanthrene, while in Ah-unresponsive mice the treatment was not effective. These results suggest that the transcription of gulonolactone oxidase gene is regulated by an Ah receptor-dependent signal transduction pathway.
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