Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2582796 | Environmental Toxicology and Pharmacology | 2016 | 8 Pages |
•The co-exposure of SiNPs and MeHg induce bradycardia and decrease the cardiac output in zebrafish embryos.•The co-exposure SiNPs and MeHg enhanced the vascular endothelial damage in Tg(fli-1:EGFP) transgenic zebrafish line.•The co-exposure of SiNPs and MeHg triggered neutrophil-mediated inflammation in Tg(mpo:GFP) transgenic zebrafish line.•Combined toxicity of SiNPs and MeHg on cardiovascular system via oxidative stress.
This study was to investigate the combined toxicity of silica nanoparticles (SiNPs) and methylmercury (MeHg) on cardiovascular system in zebrafish (Danio rerio) embryos. Ultraviolet absorption analysis showed that the co-exposure system had high absorption and stability. The dosages used in this study were based on the NOAEL level. Zebrafish embryos exposed to the co-exposure of SiNPs and MeHg did not show any cardiovascular malformation or atrioventricular block, but had an inhibition effect on bradycardia. Using o-Dianisidine for erythrocyte staining, the cardiac output of zebrafish embryos was decreased gradually in SiNPs, MeHg, co-exposure groups, respectively. Co-exposure of SiNPs and MeHg enhanced the vascular endothelial damage in Tg(fli-1:EGFP) transgenic zebrafish line. Moreover, the co-exposure significantly activated the oxidative stress and inflammatory response in neutrophils-specific Tg(mpo:GFP) transgenic zebrafish line. This study suggested that the combined toxic effects of SiNPs and MeHg on cardiovascular system had more severe toxicity than the single exposure alone.