Resistance of mouse primary microglia and astrocytes to acrylonitrile-induced oxidative stress

Samuel Caito, Marion Park, Michael Aschner

Research output: Contribution to journalArticle

Abstract

Acrylonitrile (ACN) is a widely used chemical in the production of plastics, resin, nitrile, acrylic fibers, synthetic rubber, and acrylamide. ACN is considered a Group 2B possible carcinogen in humans and is known to cause gliomas in rats. These gliomas are predominantly composed of microglia and not astrocytes. Interestingly, ACN treatment does not cause gliomas in mice, suggesting that mouse astrocytes and microglia may be resistant to ACN. We investigated the effects of ACN treatment on primary mouse microglia and astrocytes to investigate their sensitivity to the chemical. Cell viability, ACN uptake, glutathione (GSH) levels and the expression of NF-E2-related factor 2 (Nrf2) were evaluated in primary mouse microglia and astrocytes following ACN treatment. Our results indicate that mouse glial cells are resistant to ACN-induced oxidative stress. Both cell types accumulated ACN; however, there was a minor effect of ACN on cell viability in astrocytes and microglia. Nrf2 and GSH levels were unchanged in ACN-treated as compared to the untreated cells. These observations suggest that primary mouse glial cells are resistant to ACN.

Original languageEnglish (US)
Pages (from-to)120-125
Number of pages6
JournalNeuroToxicology
Volume63
DOIs
StatePublished - Dec 1 2017

Fingerprint

Acrylonitrile
Oxidative stress
Microglia
Astrocytes
Oxidative Stress
NF-E2-Related Factor 2
Glioma
Nitrile resins
Neuroglia
Cell Survival
Cells
Elastomers
Acrylic Resins
Nitriles
Acrylamide
Carcinogens
Plastics
Acrylics
Glutathione
Rats

Keywords

  • Acrylonitrile
  • Astrocyte
  • Microglia
  • Nrf2

ASJC Scopus subject areas

  • Neuroscience(all)
  • Toxicology

Cite this

Resistance of mouse primary microglia and astrocytes to acrylonitrile-induced oxidative stress. / Caito, Samuel; Park, Marion; Aschner, Michael.

In: NeuroToxicology, Vol. 63, 01.12.2017, p. 120-125.

Research output: Contribution to journalArticle

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