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Related Experiment Videos

Morphine enhances macrophage apoptosis

P C Singhal1, P Sharma, A A Kapasi

  • 1Department of Medicine, Long Island Jewish Medical Center, New Hyde Park, NY 11040, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|February 20, 1998
PubMed
Summary
This summary is machine-generated.

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Morphine triggers programmed cell death (apoptosis) in macrophages, impairing immune function. This mechanism involves nitric oxide production and key proteins like p53 and Bax, potentially explaining immune compromise in opiate addiction.

Area of Science:

  • Immunology
  • Pharmacology
  • Cell Biology

Background:

  • Morphine is known to reduce macrophage numbers and phagocytic capacity.
  • The precise mechanisms by which morphine affects macrophage function are not fully understood.

Purpose of the Study:

  • To investigate the effect of morphine on macrophage apoptosis.
  • To elucidate the molecular pathways involved in morphine-induced macrophage apoptosis.

Main Methods:

  • In vivo and in vitro studies using rat and murine macrophages, as well as human monocytes.
  • Assays for DNA fragmentation, apoptosis, nitric oxide (NO) production, and protein/mRNA expression (p53, Bax, iNOS).
  • Use of NO synthase inhibitors (L-NAME, L-NMMA) and an ICE-1 inhibitor.

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Main Results:

  • Morphine induced DNA fragmentation and apoptosis in macrophages in a dose-dependent manner.
  • Morphine increased nitric oxide (NO) production and inducible NO synthase (iNOS) expression.
  • Apoptosis was attenuated by NO synthase inhibitors, suggesting NO mediation.
  • Morphine promoted p53 and Bax protein synthesis, and apoptosis was inhibited by an ICE-1 inhibitor.
  • These findings indicate a pathway involving p53, Bax, and ICE-1 in morphine-induced apoptosis.

Conclusions:

  • Morphine induces macrophage apoptosis through a pathway involving nitric oxide generation.
  • The induction phase involves p53 accumulation, and the effector phase involves Bax and ICE-1 activation.
  • Morphine may compromise immune function in patients by promoting macrophage apoptosis.