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Experimental Analysis of Apoptotic Thymocyte Engulfment by Macrophages
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Published on: May 24, 2019

Extract of motorcycle exhaust particles induced macrophages apoptosis by calcium-dependent manner

Chen-Chen Lee1, Jaw-Jou Kang

  • 1Institute of Toxicology, College of Medicine, National Taiwan University, 1 Jen-Ai Road, Section 1, Taipei, Taiwan, ROC.

Chemical Research in Toxicology
|December 17, 2002
PubMed

Insights

Motorcycle exhaust particles (MEP) induce macrophage cell death (apoptosis) by disrupting calcium levels and increasing oxidative stress. These findings highlight the immune system risks associated with air pollution from fossil fuels.

Area of Science:

  • Environmental Science
  • Immunology
  • Toxicology

Background:

  • Environmental pollutants from fossil fuel combustion are known to harm the immune system, increasing allergic reactions and respiratory damage.
  • Motorcycle exhaust particles (MEP) are a significant component of air pollution.

Purpose of the Study:

  • To investigate the cytotoxic effects of motorcycle exhaust particles (MEP) on macrophages.
  • To elucidate the mechanisms by which MEP induces cell apoptosis in macrophages.

Main Methods:

  • Collection and extraction of MEP from a two-stroke engine.
  • Assessment of MEP cytotoxicity on RAW 264.7 cells, murine peritoneal macrophages, and rat alveolar macrophages.
  • Investigation of the role of calcium ions, mitochondria, and oxidative stress in MEP-induced apoptosis using various inhibitors and chelators.
  • Measurement of intracellular calcium concentration ([Ca(2+)](i)) using Fura-2/AM.

Main Results:

  • MEP demonstrated cytotoxicity and induced apoptosis in all tested macrophage types.
  • Inhibitors of mitochondrial permeability transition, calcium chelators (BAPTA-AM, EGTA), and antioxidants attenuated MEP-induced apoptosis, with BAPTA-AM being most effective.
  • MEP caused a sustained increase in intracellular calcium concentration ([Ca(2+)](i)), involving both extracellular influx and intracellular release.
  • MEP exposure led to decreased mitochondrial membrane potential and increased oxidative stress in RAW 264.7 cells.

Conclusions:

  • Motorcycle exhaust particles contain chemicals that induce macrophage apoptosis.
  • The apoptosis is mediated through a calcium-dependent pathway, involving both calcium influx and release from internal stores.
  • MEP-induced apoptosis is associated with mitochondrial dysfunction and oxidative stress, contributing to immune system damage.

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