Báo cáo Y học: Excessive vitamin A toxicity in mice genetically deficient in either alcohol dehydrogenase Adh1 or Adh3
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Alcohol dehydrogenase (ADH) deficiency results indecreased retinol utilization, but it is unclear what physio-logical roles the several known ADHs play in retinoidsignaling. Here, Adh1, Adh3,andAdh4null mutant micehave been examined following acute and chronic vitamin Aexcess. Following an acute dose of retinol (50 mgÆkg)1),metabolism of retinol to retinoic acid in liver was reduced10-fold inAdh1mutants and 3.8-fold inAdh3mutants, butwas not significantly reduced inAdh4mutants.
Nội dung trích xuất từ tài liệu:
Báo cáo Y học: Excessive vitamin A toxicity in mice genetically deficient in either alcohol dehydrogenase Adh1 or Adh3
Nội dung trích xuất từ tài liệu:
Báo cáo Y học: Excessive vitamin A toxicity in mice genetically deficient in either alcohol dehydrogenase Adh1 or Adh3
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