Could the endogenous opioid, morphine, prevent neural stem cell proliferation?

Med Hypotheses. 2011 Feb;76(2):225-9. doi: 10.1016/j.mehy.2010.10.002. Epub 2010 Nov 3.

Abstract

In spite of widespread use of morphine to treat pain in patients, little is known about the effects of this opioid on many cells including stem cells. Moreover the studies have been shown controversial results about morphine effects on several kinds of cells. It is well-known that morphine exposure could decrease testosterone levels in brain and spinal cord. Morphine could increase the activity of 5α-redutase, the enzyme that converts testosterone into its respective 5α-redutase derivative dihydrotestosterone (DHT). Also it could increase aromatase activity that converts testosterone to estradiol. Proliferation of neural stem cells was observed in human stem cells after exposure to certain combinations of steroids especially testosterone. On the other hand DHT has negative effect in neural stem cell reproduction. Morphine induces over-expression of p53 gene that could mediate stem cell apoptosis. Therefore we hypothesized that due to reduction in the testosterone levels, elevation in the DHT levels, and over-expression of p53 gene, morphine could prevent neural stem cell proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3-Oxo-5-alpha-Steroid 4-Dehydrogenase / metabolism
  • 5-alpha Reductase Inhibitors / pharmacology
  • Animals
  • Apoptosis
  • Cell Proliferation
  • Dihydrotestosterone / metabolism
  • Genes, p53
  • Humans
  • Models, Biological
  • Morphine / pharmacology*
  • Neural Stem Cells / drug effects*
  • Neurodegenerative Diseases / prevention & control*
  • Neurodegenerative Diseases / therapy
  • Rats
  • Regeneration
  • Testosterone / metabolism

Substances

  • 5-alpha Reductase Inhibitors
  • Dihydrotestosterone
  • Testosterone
  • Morphine
  • 3-Oxo-5-alpha-Steroid 4-Dehydrogenase