Alcohol dehydrogenase (ADH) deficiency results in decreased retinol utilization, but it is unclear what physio-logical roles the several known ADHs play in retinoid signaling. Here, Adh1, Adh3,andAdh4null mutant mice have been examined following acute and chronic vitamin A excess. Following an acute dose of retinol (50 mgÆkg )1 ), metabolism of retinol to retinoic acid in liver was reduced 10-fold inAdh1mutants and inAdh3mutants, but was not significantly reduced inAdh4mutants.
