Metallothioneins act downstream of insulin signaling to regulate toxicity of outdoor fine particulate matter (PM(2.5)) during Spring Festival in Beijing in nematode Caenorhabditis elegans

金属硫蛋白在胰岛素信号传导的下游发挥作用,调节春节期间北京室外细颗粒物(PM(2.5))对线虫秀丽隐杆线虫的毒性。

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Abstract

In this study, we performed the toxicological assessment of outdoor PM(2.5) collected from Beijing during Spring Festival using the in vivo assay system of Caenorhabditis elegans. Acute exposure to outdoor PM(2.5) at a concentration of 10 mg L(-1) and prolonged exposure to outdoor PM(2.5) at concentrations of 0.1-10 mg L(-1) decreased locomotion behavior and caused significant induction of intestinal ROS production. Meanwhile, outdoor PM(2.5) exposure induced significant expression of gene (mtl-1 and mtl-2) encoded metallothioneins in the intestine. Mutation of the mtl-1 or mtl-2 gene resulted in a susceptible property of nematodes to outdoor PM(2.5) toxicity. Genetic assays suggested that mtl-1 and mtl-2 genes acted downstream of the daf-16 gene encoding a FOXO transcriptional factor and daf-2 gene encoding an insulin receptor in the insulin signaling pathway to regulate outdoor PM(2.5) toxicity. DAF-2 further acted upstream of DAF-16 and suppressed the function of DAF-16 to regulate outdoor PM(2.5) toxicity. Therefore, we identified a signaling cascade of DAF-2-DAF-16-MTL-1/2 in the control of outdoor PM(2.5) toxicity in nematodes. Our study provides an important molecular basis for the potential toxicity of outdoor PM(2.5) during Spring Festival in Beijing in nematodes. Especially, our study will highlight the potential adverse effects of outdoor PM(2.5) during Spring Festival on environmental organisms.

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