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

- We addressed glial cell viability, ACN uptake, glutathione (GSH) levels and the expression of NF-E2-related factor 2 (Nrf2) in response to ACN treatment.
- Mouse glial cells were 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.

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.