Chronic ethanol administration enhances retinoic acid and triiodothyronine receptor expression in mouse liver

FEBS Lett. 1993 Sep 27;331(1-2):119-22. doi: 10.1016/0014-5793(93)80309-i.

Abstract

Chronic alcoholism induces perturbations of storage and metabolization of retinol and related compounds. After 6 months of ethanol consumption we have observed in mouse liver an increased expression of Tri-iodothyronine receptors (TR) while the expression of retinoic acid (RA) receptors (RAR) was unaffected. After 10 months of alcoholization the TR expression was strongly increased and the RAR expression was also increased. At this time the activity of aldehyde dehydrogenase and that of alcohol dehydrogenase, two enzymes involved in biosynthesis of RA from retinol, were similar in the liver of alcoholized and pair-fed mice. Thus it can be hypothesized that (i) the change of RAR expression was, at least in part, the result of a change of TR expression (result in agreement with previous data), (ii) the increased expression of RAR could induce apoptosis and subsequently liver necrosis.

MeSH terms

  • Alcohol Dehydrogenase / metabolism
  • Alcoholism / metabolism*
  • Aldehyde Dehydrogenase / metabolism
  • Animals
  • Ethanol / administration & dosage
  • Ethanol / pharmacology*
  • Liver / drug effects*
  • Liver / enzymology
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • RNA, Messenger / metabolism
  • Receptors, Retinoic Acid / biosynthesis*
  • Receptors, Retinoic Acid / genetics
  • Receptors, Thyroid Hormone / biosynthesis*
  • Receptors, Thyroid Hormone / genetics

Substances

  • RNA, Messenger
  • Receptors, Retinoic Acid
  • Receptors, Thyroid Hormone
  • Ethanol
  • Alcohol Dehydrogenase
  • Aldehyde Dehydrogenase