Abstract
Oxidative stress has been proven as one of the most critical regulatory mechanisms involved in fine Particulate Matter- (PM(2.5)-) mediated toxicity. For a better understanding of the underlying mechanisms that enable oxidative stress to participate in PM(2.5)-induced toxic effects, the current study explored the effects of oxidative stress induced by PM(2.5) on UPR and lifespan in C. elegans. The results implicated that PM(2.5) exposure induced oxidative stress response, enhanced metabolic enzyme activity, activated UPR, and shortened the lifespan of C. elegans. Antioxidant N-acetylcysteine (NAC) could suppress the UPR through reducing the oxidative stress; both the antioxidant NAC and UPR inhibitor 4-phenylbutyric acid (4-PBA) could rescue the lifespan attenuation caused by PM(2.5), indicating that the antioxidant and moderate proteostasis contribute to the homeostasis and adaptation to oxidative stress induced by PM(2.5).