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Bystander effects induced by chemicals and ionizing radiation: evaluation of changes in gene expression of downstream

Rajalakshmi Asur1, Mamtha Balasubramaniam, Brian Marples

  • 1Department of Biological Sciences, Wayne State University, 5047 Gullen Mall, Suite 1370, Detroit, MI 48202-3917, USA.

Mutagenesis
|February 5, 2010
PubMed

Insights

Chemicals like mitomycin C (MMC) and phleomycin (PHL) can induce bystander effects, altering gene expression in non-exposed cells. These effects, particularly from MMC and radiation, involve mitogen-activated protein kinase (MAPK) pathways, suggesting a general stress response.

Area of Science:

  • Cellular and Molecular Biology
  • Radiation Biology
  • Toxicology

Background:

  • Radiation-induced bystander effects are well-studied, often involving mitogen-activated protein kinase (MAPK) pathways.
  • Chemical induction of bystander effects and their underlying molecular mechanisms remain largely unexplored.
  • Previous work established mitomycin C (MMC) and phleomycin (PHL) as inducers of bystander effects in human lymphoblastoid cells.

Purpose of the Study:

  • To investigate molecular mechanisms of chemical bystander effects.
  • To examine changes in MAPK target gene expression following bystander exposure to MMC, PHL, or ionizing radiation.
  • To determine if chemical bystander effects involve MAPK pathways.

Main Methods:

  • Assessed expression changes of 18 MAPK target genes.
  • Evaluated gene expression at various time points after direct or bystander exposure to MMC, PHL, and ionizing radiation.
  • Analyzed gene expression data in the context of MAPK pathway combinations.

Main Results:

  • Statistically significant gene expression changes were observed following direct exposure to all agents.
  • Bystander cells exposed to MMC or ionizing radiation showed significant increases in MAPK target gene expression.
  • Bystander cells exposed to PHL did not exhibit significant increases in MAPK target gene expression, unlike radiation.
  • PHL responses in bystander cells did not mimic radiation responses.

Conclusions:

  • Bystander effects involve changes in MAPK proteins and their downstream targets.
  • MMC and ionizing radiation induce bystander effects that activate MAPK target genes.
  • Bystander effects appear to be a component of a generalized cellular stress response.

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