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The toxicity of ZnO nanoparticles (NPs) has been widely investigated because of their extensive use in consumer products. The mechanism of the toxicity of ZnO NPs to algae is unclear, however, and it is difficult to differentiate between particle-induced toxicity and the effect of dissolved Zn(2+). In the work discussed in this paper we investigated particle-induced toxicity and the effects of dissolved Zn(2+) by using the chiral perturbation approach with dichlorprop (DCPP) as chiral perturbation factor. The results indicated that intracellular zinc is important in the toxicity of ZnO NPs, and that ZnO NPs cause oxidative damage. According to dose-response curves for DCPP and the combination of ZnO NPs with (R)-DCPP or (S)-DCPP, the toxicity of DCPP was too low to perturb the toxicity of ZnO NPs, so DCPP was suitable for use as chiral perturbation factor. The different glutathione (GSH) content of algal cells exposed to (R)-DCPP or (S)-DCPP correlated well with different production of reactive oxygen species (ROS) after exposure to the two enantiomers. Treatment of algae with ZnO NPs and (R)-DCPP resulted in reduced levels of GSH and the glutathione/oxidized glutathione (GSH/GSSG) ratio in the cells compared with the control. Treatment of algae with ZnO NPs and (S)-DCPP, however, resulted in no significant changes in GSH and GSH/GSSG. Moreover, trends of variation of GSH and GSH/GSSG were different when algae were treated with ZnSO4·7H2O and the two enantiomers. Overall, the chiral perturbation approach revealed that NPs aggravated generation of ROS and that released Zn(2+) and NPs both contribute to the toxicity of ZnO NPs.

Fascinating super paramagnetic uniqueness of iron oxide particles at nano-scale level make them extremely useful in the state of the art therapies, equipments, and techniques. Cobalt ferrite (CoFe O ) magnetic nanoparticles (MNPs) are extensively used in nano-based medicine and electronics, results in extensive discharge and accumulation into the environment. However, very limited information is available for their endocrine disrupting potential in aquatic organisms. In this study, the thyroid endocrine disrupting ability of CoFe O NPs in Zebrafish larvae for 168-h post fertilization (hpf) was evaluated. The results showed the elevated amounts of T4 and T3 hormones by malformation of hypothalamus pituitary axis in zebrafish larvae. These elevated levels of whole body THs leads to delayed hatching, head and eye malformation, arrested development, and alterations in metabolism. The influence of THs disruption on ROS production and change in activities of catalase (CAT), mu-glutathione s-transferase (mu-GST), and acid phosphatase (AP) were also studied. The production of significantly higher amounts of in vivo generation of ROS leads to membrane damage and oxidative stress. Presences of NPs and NPs agglomerates/aggregates were also the contributing factors in mechanical damaging the membranes and physiological structure of thyroid axis. The increased activities of CAT, mu-GST, and AP confirmed the increased oxidative stress, possible DNA, and metabolic alterations, respectively. The excessive production of in vivo ROS leads to severe apoptosis in head, eye, and heart region confirming that malformation leads to malfunctioning of hypothalamus pituitary axis. ROS-induced oxidative DNA damage by formation of 8-OHdG DNA adducts elaborates the genotoxicity potential of CoFe O NPs. This study will help us to better understand the risk and assessment of endocrine disrupting potential of nanoparticles. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 2068-2080, 2016.

Isopyrazam (IPZ) is a broad spectrum succinate dehydrogenase inhibitor fungicide. Little is known about its potential ecological risks of aquatic organisms recently. The present study examined the embryonic development effects of zebrafish exposed to IPZ under static condition using a fish embryo toxicity test. The lowest observed effect concentration of IPZ was 0.025 mg/L in 4-day exposure. Developmental abnormalities, including edema, small head deformity, body deformation and decreased pigmentation, and mortality were observed in zebrafish embryos of 0.05 mg/L and higher concentrations, which shown concentration dependency. The heart rate of zebrafish was disrupted by IPZ. Moreover, enzyme and gene experiments shown that IPZ exposure caused oxidative stress of zebrafish. Furthermore, it induced a decrease of succinate dehydrogenase (SDH) enzyme activity and gene transcription level in zebrafish larvae. It can be speculated that IPZ may have a lethal effect on zebrafish, which is accompanied by decreased SDH activity, oxidative stress, and abnormality. These results provide toxicological data about the IPZ on aquatic non-target organisms, which could be useful for further understanding potential environmental risks.