Nicotinamide adenine dinucleotide-dependent retinoic acid formation from retinol in the human gastric mucosa: inhibition by ethanol, acetaldehyde, and H2 blockers

Alcohol Clin Exp Res. 2001 Jun;25(6 Suppl):24S-8S. doi: 10.1097/00000374-200106001-00007.


All-trans retinoic acid formation from all-trans retinol (vitamin A) in the human gastric mucosa was studied. When all-trans retinol and the human gastric mucosa were incubated together, all-trans retinoic acid was formed in the presence of nicotinamide adenine dinucleotide (NAD). When the NAD was not added, hardly any formation was observed. The formation of all-trans retinoic acid tended to be attenuated by 10 mM ethanol. Moreover, it was significantly attenuated in a concentration-dependent manner by ethanol at concentrations of 100 mM and above. Acetaldehyde at concentrations of 50 microM and above also significantly attenuated its formation in a concentration-dependent manner. Some H2 blockers, which include ranitidine hydrochloride and cimetidine, significantly attenuated the formation of all-trans retinoic acid, whereas famotidine failed to suppress it. There is an NAD-dependent pathway by which all-trans retinoic acid is produced from all-trans retinol in the human gastric mucosa. Inhibitors of alcohol dehydrogenase, which include ethanol and some H2 blockers, and of aldehyde dehydrogenase, which include acetaldehyde, inhibit its production.

MeSH terms

  • Acetaldehyde / pharmacology*
  • Adult
  • Cimetidine / pharmacology
  • Ethanol / pharmacology*
  • Gastric Mucosa / drug effects*
  • Gastric Mucosa / metabolism
  • Histamine H2 Antagonists / pharmacology*
  • Humans
  • Middle Aged
  • NAD / pharmacology
  • Ranitidine / pharmacology
  • Tretinoin / metabolism*
  • Vitamin A / metabolism*


  • Histamine H2 Antagonists
  • NAD
  • Vitamin A
  • Ethanol
  • Tretinoin
  • Cimetidine
  • Ranitidine
  • Acetaldehyde