Impacts of isopyrazam exposure on the development of early-life zebrafish (Danio rerio).

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.

The embryonic developmental effect of sedaxane on zebrafish (Danio rerio).

The succinate dehydrogenase inhibitor (SDHI) fungicides have been extensively used in agriculture, and some of their potential ecological risks to aquatic organisms have been demonstrated recently. Sedaxane (SDX) is a broad spectrum SDHI fungicide. Despite being extensively used in environment, little is known about its potential developmental effect in zebrafish embryo. This study examined the effects of which SDX triggered in zebrafish through embryonic development assessments. Results show that SDX induced mortality, hatch delay and failure in zebrafish embryos, which were concentration dependent. In addition, several developmental abnormalities were observed at 2 mg/L and higher concentrations, including edema, microcephaly, body deformation, and swim bladder not fully inflated. SDX exposure influenced reactive oxygen species, malondialdehyde, peroxidase, glutathione S-transferase, superoxide dismutase and glutathione in live larvae, which indicated that oxidative stress was caused in zebrafish. Furthermore, SDX induced decrease of succinate dehydrogenase activity in zebrafish larvae. These results provide toxicological data of SDX on developing zebrafish embryo, which could be help for further understanding the potential risk on the environment.

Probing the interaction induced conformation transitions in acid phosphatase with cobalt ferrite nanoparticles: Relation to inhibition and bio-activity of Chlorella vulgaris acid phosphatase.

The present study explored the interaction and kinetics of cobalt ferrite nanoparticles (NPs) with acid phosphatase (ACP) by utilizing diverse range of spectroscopic techniques. The results corroborate, the CoFe2O4 NPs cause fluorescence quenching in ACP by static quenching mechanism. The negative values of van't Hoff thermodynamic expressions (ΔH=-0.3293Jmol(-1)K(-1) and ΔG=-3.960kJmol(-1)K(-1)) corroborate the spontaneity and exothermic nature of static quenching. The positive value of ΔS (13.2893Jmol(-1)K(-1)) corroborate that major contributors of higher and stronger binding affinity among CoFe2O4 NPs with ACP were electrostatic. In addition, FTIR, UV-CD, UV-vis spectroscopy and three dimensional fluorescence (3D) techniques confirmed that CoFe2O4 NPs binding induces microenvironment perturbations leading to secondary and tertiary conformation changes in ACP to a great extent. Furthermore, synchronous fluorescence spectroscopy (SFS) affirmed the comparatively significant changes in microenvironment around tryptophan (Trp) residue by CoFe2O4 NPs. The effect of CoFe2O4 NPs on the activation kinetics of ACP was further examined in Chlorella vulgaris. Apparent Michaelis constant (Km) values of 0.57 and 26.5mM with activation energy values of 0.538 and 3.428kJmol(-1) were determined without and with 200µM CoFe2O4 NPs. Apparent Vmax value of -7Umml(-1) corroborate that enzyme active sites were completely captured by the NPs leaving no space for the substrate. The results confirmed that CoFe2O4 NPs ceased the activity by unfolding of ACP enzyme. This suggests CoFe2O4 NPs perturbed the enzyme activity by transitions in conformation and hence the metabolic activity of ACP. This study provides the pavement for novel and simple approach of using sensitive biomarkers for sensing NPs in environment.

Assessment of thyroid endocrine system impairment and oxidative stress mediated by cobalt ferrite (CoFe2 O4 ) nanoparticles in zebrafish larvae.

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 (CoFe2 O4 ) 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 CoFe2 O4 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 CoFe2 O4 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.

Toxicity of cobalt ferrite (CoFe2O4) nanobeads in Chlorella vulgaris: interaction, adaptation and oxidative stress.

The potential toxicity of CoFe2O4 nanobeads (NBs) in Chlorella vulgaris was observed up to 72h. Algal cell morphology, membrane integrity and viability were severely compromised due to adsorption and aggregation of NBs on algal surfaces, release of Fe(3+) and Co(2+) ions and possible mechanical damage by NBs. Interactions with NBs and effective decrease in ions released by aggregation and exudation of algal cells as a self defense mechanism were observed by Fourier transform infrared attenuated total reflectance (FTIR-ATR) and inductively coupled plasma mass spectrometry (ICP-MS). The results corroborated CoFe2O4 NBs induced ROS triggered oxidative stress, leading to a reduction in catalase activity, activation of the mutagenic glutathione s-transferase (mu-GST) and acid phosphatase (AP) antioxidant enzymes, and an increase in genetic aberrations, metabolic and cellular signal transduction dysfunction. Circular dichroism (CD) spectra indicated the weak interactions of NBs with BSA, with slight changes in the α-helix structure of BSA confirming conformational changes in structure, hence the potential for functional interactions with biomolecules. Possible interferences of CoFe2O4 NBs with assay techniques and components indicated CoFe2O4 NBs at lower concentration do not show any significant interference with ROS, catalase, mu-GST and no interference with CD measurements. This study showed ROS production is one of the pathways of toxicity initiated by CoFe2O4 NBs and illustrates the complex processes that may occur between organisms and NBs in natural complex ecosystem.

An in vivo evaluation of acute toxicity of cobalt ferrite (CoFe2O4) nanoparticles in larval-embryo Zebrafish (Danio rerio).

The broad spectrum applications of CoFe2O4 NPs have attracted much interest in medicine, environment and industry, resulting in exceedingly higher exposures to humans and environmental systems in succeeding days. Their health effects and potential biological impacts need to be determined for risk assessment. Zebrafish (Danio rerio) embryos were exposed to environmentally relevant doses of nano-CoFe2O4 (mean diameter of 40nm) with a concentration range of 10-500µM for 96h. Acute toxic end points were evaluated by survival rate, malformation, hatching delay, heart dysfunction and tail flexure of larvae. Dose and time dependent developmental toxicity with severe cardiac edema, down regulation of metabolism, hatching delay and tail/spinal cord flexure and apoptosis was observed. The biochemical changes were evaluated by ROS, Catalase (CAT), Lipid peroxidation (LPO), Acid phophatase (AP) and Glutatione s- transferase (GST). An Agglomeration of NPs and dissolution of ions induces severe mechanical damage to membranes and oxidative stress. Severe apoptosis of cells in the head, heart and tail region with inhibition of catalase confirms ROS induced acute toxicity with increasing concentration. Increased activity of GST and AP at lower concentrations of CoFe2O4 NPs demonstrates the severe oxidative stress. Circular dichroism (CD) spectra indicated the weak interactions of NPs with BSA and slight changes in α-helix structure. In addition, CoFe2O4 NPs at lower concentrations do not show any considerable interference with assay components and analytical instruments. The results are possible elucidation of pathways of toxicity induced by these particles, as well as contributing in defining the protocols for risk assessment of these nanoparticles.

Evaluation of the toxicity of ZnO nanoparticles to Chlorella vulgaris by use of the chiral perturbation approach.

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.