Keywords: 
• acrylonitrile /
• rats /
• iNOS /
• p38 MAPK

Abstract: To investigate the effects of iNOS/p38 MAPK signaling pathway induced via acrylonitrile (ACN) on brain injury, which are beneficial to provide the basis for neurological toxicity of ACN, we randomly distributed fifty healthy adult male SD rats into five groups of 10 rats each. After adaptive feeding for one week, rats in the exposed groups were respectively treated with doses of 12.5, 25.0 and 50.0 mg·kg^-1 of ACN via gavage, and the control group was given corn oil. After being treated with 50.0 mg·kg^-1 ACN 30 minutes, rats in the N-acetylcysteine (NAC) group were treated with 300.0 mg·kg^-1 NAC. All the rats were gavaged once a day, six days per week. The final body weights were recorded after 13 weeks, then all rats were sacrificed. The contents of nitric oxide (NO) and the activities of total nitric oxide synthase (tNOS) in rats brains were detected. The expression levels of inducible or immunological nitric oxide synthase (iNOS), phospho-p38 and p38 proteins were also measured by Western blot. Results showed that the relative organ weights of the rat brain tissues in the low, medium and high dose groups were significantly lower than that in the control group, but no significant difference between NAC group and the high dose group. Compared with the control group, marked increase of NO level and the activities of tNOS in the high group were observed. However, there was no significant difference in the level of NO and the activities of tNOS between NAC group and the high dose group. And the levels of iNOS, phospho-p38 proteins and the ratios of phospho-p38 protein to p38 protein in the high dose group were significantly higher than that in the control and NAC group. The activation of iNOS/p38 MAPK signaling pathway may be one of the mechanisms of brain injury induced by ACN in rats.