Inhibition by nicotinic acid of hepatic steatosis and alcohol dehydrogenase in ethanol-treated rats

Herman Baker, Anita Luisada-Opper, Michael F. Sorrell, Allan D. Thomson, Oscar Frank

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

A single intoxicating dose of ethanol (6.0 g/kg) depressed the NAD: NADH2 ratio and increased the NADPH2: NADP ratio in rat liver. Nicotinic acid (NA) treatment prevented the accumulation of nonesterified fatty acid (NEFA), total fats, and neutral fats in the liver of rats given ethanol (EtOH); it also kept blood EtOH elevated. We postulate that NA acted by blocking EtOH oxidation-a block apparently exerted by inhibition of alcohol dehydrogenase (ADH), mediator of the principal oxidative pathway of ethanol metabolism. It was inferred that NA inhibits the enzyme by binding at the adenosine diphosphate ribose site since the addition of Zn2+ in vitro failed to reverse the NA inhibition of rat liver ADH. Blockage at the aforementioned site would thus inhibit coenzyme (NAD) binding to the apoenzyme, resulting in a block in the EtOH oxidation.

Original languageEnglish (US)
Pages (from-to)106-112
Number of pages7
JournalExperimental and Molecular Pathology
Volume19
Issue number1
DOIs
StatePublished - Aug 1973
Externally publishedYes

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Clinical Biochemistry

Fingerprint

Dive into the research topics of 'Inhibition by nicotinic acid of hepatic steatosis and alcohol dehydrogenase in ethanol-treated rats'. Together they form a unique fingerprint.

Cite this