Comparative Toxicity of TiO2 and Sn-Doped TiO2 Nanoparticles in Zebrafish After Acute and Chronic Exposure.

This study was conducted to assess the toxicological potential of synthesized pure and Sn-doped TiO2 NPs (Sn-TiO2 NPs) in zebrafish after acute and chronic exposure. The pure TiO2 NPs, 4%, and 8% Sn-TiO2 NPs were synthesized and characterized using X-ray diffraction, Scanning Electron Microscope, diffuse reflectance spectra, dynamic light scattering, and zeta potential analyses. The pure TiO2 NPs, 4%, and 8% Sn-TiO2 NPs were spherical with average sizes of about 40, 28, and 21 nm, respectively, indicating significant size reduction of TiO2 NPs following Sn doping. According to our results, the LC50-96h increased in the order of 8% Sn-TiO2 NPs (45 mg L-1) < 4% Sn-TiO2 NPs (80.14 mg L-1) < pure TiO2 NPs (105.47 mg L-1), respectively. Exposure of fish to Sn-TiO2 NPs after 30 days resulted in more severe histopathological alterations in gills, liver, intestine, and kidneys than pure TiO2 NPs. Furthermore, Sn-doping significantly elevated malondialdehyde levels and micronuclei frequency, indicating increased oxidative stress and genotoxicity. Expression analysis revealed altered expression of various genes, including upregulation of pro-apoptotic Bax gene and downregulation of anti-apoptotic Bcl-2 gene, suggesting potential induction of apoptosis in response to Sn-doped NPs. Additionally, antioxidant genes (Gpx, Sod, Cat, and Ucp-2) and stress response gene (Hsp70) showed altered expression, suggesting complex cellular responses to mitigate the toxic effects. Overall, this study highlights the concerning impact of Sn-doping on the toxicity of TiO2 NPs in zebrafish and emphasizes the need for further research to elucidate the exact mechanisms underlying this enhanced toxicity.

Oxidative stress, genotoxic effects, and other damages caused by chronic exposure to silver nanoparticles (Ag NPs) and zinc oxide nanoparticles (ZnO NPs), and their mixtures in zebrafish (Danio rerio).

This study assessed the oxidative stress impacts of Ag NPs and ZnO NPs and their mixtures in zebrafish (Danio rerio). Zebrafish were exposed to sublethal concentrations of each NP and a mixture for 28 days followed by a 28-day recovery period (without NP exposure) and measurements made on hepatic levels of antioxidant enzymes (CAT, SOD, and GPx), MDA levels, expression of the genes for the Hsp70 and Hsp90, and MT, blood biochemical parameters (total protein, globulin, albumin, AST, ALT, ALP, and LDH), and genotoxicity in erythrocytes (via measurement of micronuclei (MN) and nuclear (NA) abnormalities). There was a tendency for an increase in the variation in the responses of antioxidant defense systems and there were higher MDA levels with increasing exposure concentration of Ag NPs and with increasing exposure time. Total protein, globulin, and albumin decreased during the exposure period, especially on the days of 28. Moreover, levels of AST and LDH increased significantly in the NPs co-exposure treatments, while levels of ALT and ALP significantly decreased. The highest expression levels for these genes occurred on day 14 and in the NPs co-exposure treatments. For exposure to both NPs individually and as a mixture, the frequency of MN and other NA were significantly increased (p < 0.05). During the recovery periods, most of the effects seen were reduced, most notably in the individual NPs treatments. The overall results suggest that the toxic effects of Ag NPs and ZnO NPs in combination significantly increase their toxicity in zebrafish.

Toxicity of Silver Nanoparticles in the Presence of Zinc Oxide Nanoparticles Differs for Acute and Chronic Exposures in Zebrafish.

We assessed the acute toxicity effects (96 h) of silver nanoparticles (Ag NPs) and zinc oxide nanoparticles (ZnO NPs) and chronic (28 d) exposure to Ag NPs, including in combination with ZnO NPs. In the chronic studies, we further assessed the toxicokinetics and bioaccumulation of Ag and the resulting histopathological effects in the gill, intestine, and liver of zebrafish. Co-exposures with ZnO NPs reduced the toxicity of Ag NPs for acute (lethality) but enhanced the toxicity effects (tissue histopathology) for chronic exposures. The histological lesions for both NPs exposures in the gill included necrosis and fusion of lamellae, for the intestine necrosis and degeneration, and in the liver, mainly necrosis. The severity of the histological lesions induced by the Ag NPs was related to the amount of accumulated Ag in the zebrafish organs. The Ag accumulation in different organs was higher in the presence of ZnO NPs in the order of the gill > intestine > liver. Depuration kinetics illustrated the lowest half-life for Ag occurred in the gill and for the combined exposure of Ag with ZnO NPs. Our findings illustrate that in addition to tissue, time, and exposure concentration dependencies, the Ag NPs toxicity can also be influenced by the co-exposure to other NPs (here ZnO NPs), emphasizing the need for more combination exposure effects studies for NPs to more fully understand their potential environmental health risks.

Toxicological effects of Ag2O and Ag2CO3 doped TiO2 nanoparticles and pure TiO2 particles on zebrafish (Danio rerio).

In this study, the toxic effects of silver oxide and silver carbonate doped TiO2 nanoparticles (Ag2O-TiO2 NPs and Ag2CO3-TiO2NPs), TiO2 nanoparticles (TiO2 NPs), and bulk TiO2 on gene expression, lipid peroxidation, genotoxicity, and histological alterations in zebrafish (Danio rerio) was assessed. The physicochemical properties of the synthesized nanoparticles were evaluated by X-ray diffraction (XRD), Scanning Electron Microscope (SEM), diffuse reflectance spectroscopy (DRS), dynamic light scattering (DLS), and Zeta potential analyses. TiO2NPs after doping with Ag showed shift to higher wavelengths and decrease of band gap energy. Also, remarkable reduction in the size of Ag-doped TiO2NPs in comparison with the TiO2 NPs was observed. According to our results, acute toxicity increased in the order of bulk TiO2 < TiO2 NPs < Ag2O-TiO2NPs < Ag2CO3-TiO2NPs, respectively. Results of sub-lethal experiments after 30 days of exposure, showed higher expression of Gpx, Hsp70, Ucp-2, and Bax genes, and lower expression of Bcl-2 gene in Ag-doped TiO2NPs than pure TiO2 particles (TiO2 NPs and bulk TiO2) treatments (p < 0.05). However, the mRNA levels of SOD and CAT genes were significantly higher in pure TiO2 particles than doped TiO2NPs (p < 0.05). Moreover, levels of malondialdehyde, abnormalities of peripheral blood cells and severity of histological lesions in liver, gill, intestine and kidney tissues were more evident in Ag-dopedTiO2 NPs than pure TiO2 particles. It can be concluded that Ag doping of TiO2 NPs significantly increased their toxicity and resulted in more histological lesions, apoptosis and oxidative stress than pure TiO2 particles in adult zebrafish.