Acrylonitrile (ACN) like many organic solvents produce neurotoxicity by elevating brain glial fibrillary acidic protein (GFAP), a putative biomarker of astrogliosis. In this study we tested the hypothesis that sodium thiosulfate (STS) protective action against ACN-induced astrogliosis is glutathione (GSH) mediated. Male Sprague-Dawley rats were administered for 2 weeks intraperitoneal doses (50 mg/kg body weight) of the ACN, with or without STS as outline in the Methods section. Specific brain regions were tested for GFAP, GSH and glutathione-S-transferase (GST) enzyme activity. In the brain regions tested STS significantly (P</=0.05) maintained GFAP levels at the basal saline control levels, when compared to ACN-treated groups. STS also significantly (P</=0.05) increased GSH levels in these brain regions with a corresponding increased in GST enzyme activity. Although the data indicated that STS antidotal action against ACN-induced neurotoxicity is likely to involve GSH and GST activity, other complex series of mechanisms may be involved.