Titanium dioxide nanoparticles decreases bioconcentration of azoxystrobin in zebrafish larvae leading to the alleviation of cardiotoxicity

Interactions between titanium dioxide nanoparticles (n-TiO2) and pollutants in the aquatic environment may alter the bioavailability of pollutants, and thus altering their toxicity and fate. In order to investigate the bio-concentration of azoxystrobin (AZ) and its mechanism of cardiotoxicity in the presence of n-TiO2, the experiment was divided into control, n-TiO2 (100 mu g/L), AZ (40, 200 and 1000 mu g/L) and AZ (40, 200, 1000 mu g/L) +n-TiO2 groups, and the zebrafish embryos were exposed to the exposure solution until 72 h post-fertilization. Results suggested the presence of n-TiO2 notably reduced the accumulation of AZ in larvae compared with exposure to AZ alone, thereby significantly decreasing AZ-induced cardiotoxicity, including heart rate changes, pericardium edema, venous thrombosis, increased sinus venosus and bulbus arteriosus distance and changes in cardiac -related gene expression. Further studies showed that AZ +n-TiO2 together restrained total-ATPase and Ca2+- ATPase activities, while the activity of Na+K+-ATPase increased at first and then decreased. Furthermore, there were significant changes in the expressions of oxidative phosphorylation and calcium channel-related genes, suggesting mitochondrial dysfunction may be the potential mechanism of cardiotoxicity induced by AZ and n-TiO2. This study supplies a new perspective for the joint action of AZ and environmental coexisting pollutants and provides a basis for ecological risk management of pesticides.

Automated summary

The presence of titanium dioxide nanoparticles (n-TiO2) significantly reduces the accumulation of azoxystrobin (AZ) and alleviates AZ-induced cardiotoxicity. The joint action of AZ and n-TiO2 leads to mitochondrial dysfunction, which may be the potential mechanism of cardiotoxicity.