All-trans-retinoic acid induces apoptosis in Leydig cells via activation of the mitochondrial death pathway and antioxidant enzyme regulation

J Bioenerg Biomembr. 2008 Aug;40(4):315-23. doi: 10.1007/s10863-008-9156-8. Epub 2008 Jul 31.

Abstract

In addition to playing a fundamental role in diverse processes, such as vision, growth and differentiation, vitamin A and its main biologically active derivative, retinoic acid (RA), are clearly involved in the regulation of testicular functions. The present study was undertaken to examine the direct effect of RA treatment on Leydig (TM-3) cells. TM-3 cells were cultured and treated with varying concentrations of RA for 24h. High doses of RA (1-20microM) induced a decrease in cell vitality and an increase in lipid peroxidation. RA treatment also induced a corresponding increase in apoptosis in the same cells in a dose-dependent manner. Apoptosis proceeded via the mitochondrial dependent pathway, as demonstrated by the release of cytochrome c, caspase-3 enzymatic activation and DNA fragmentation. Conversely, at physiological doses (0.1-500nM) RA did not increase lipid peroxidation or cell death and resulted in an increase of antioxidant enzyme activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / metabolism*
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Cell Line
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation, Enzymologic / drug effects
  • Gene Expression Regulation, Enzymologic / physiology
  • Leydig Cells / drug effects
  • Leydig Cells / physiology*
  • Leydig Cells / ultrastructure
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mitochondria / drug effects
  • Mitochondria / physiology*
  • Oxidoreductases / metabolism*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*
  • Tretinoin / administration & dosage*

Substances

  • Antioxidants
  • Tretinoin
  • Oxidoreductases