Developmental toxicity induced by Cu(OH)(2) nanopesticide in zebrafish embryos.

The current study evaluates the adverse effects of Cu(OH)2 nanopesticide (CNPE) on the early life stages of zebrafish (Danio rerio). The developmental toxicity was determined using different parameters such as mortality (including LC50 ), hatching, heart rates, malformations, and alteration of the gene expressions. Zebrafish embryos (4 hpf-hours postfertilization) were exposed to 1.0, 2.0, 4.0, 8.0, and 16.0 mg/l CNPE doses until 96 hpf. The 96 hours LC50 was recorded at 6.258 mg/l. Seventy-two hpf total malformation index values for 2.0, 4.0, and 8.0 mg/l CNPE doses were 4.3, 7.2 and 7.9, respectively. 1.0 mg/l CNPE is not toxic for the zebrafish embryos/larvae. 2.0 to 8.0 CNPE doses caused some abnormalities in embryos/larvae morphology, including lack of body parts, tail deformities, chorda deformity, bubbled head, scoliosis, lordosis, weak or non-pigmentation, decreased heart rate and larva length. 16.0 mg/l CNPE caused mortality in 72 hpf. The expression levels of seven immune system-related genes (il-1β, il-8, cebp, tlr4, hsp70, NF-kB, and mtf-1) were examined. The transcription level of il-1β, il-8, tlr4, hsp70, and NF-kB genes significantly increased in the CNPE exposure groups. While the expression of the mtf-1 gene considerably decreased, the cebp gene expression level did not change in the 4.0 and 8.0 mg/l CNPE doses. In conclusion, CNPE could induce developmental toxicity with malformations in embryos/larvae and alter the gene expression.

Aksakal FI ，Sisman T 《-》

Impact of copper oxide nanoparticles (CuO NPs) exposure on embryo development and expression of genes related to the innate immune system of zebrafish (Danio rerio).

CuO NPs are nanomaterials with catalytic activity and unique thermo-physical properties used in different fields such as sensors, catalysts, surfactants, batteries, antimicrobials and solar energy transformations. Because of its wide field of use, these nanoparticles accumulate in the aquatic environment and thus lead to toxic effects on aquatic organisms. The toxicological findings about CuO NPs are controversial and these effects of CuO NPs on aquatic organisms have not been elucidated in detail. Therefore, the aim of this study was to investigate the toxic effect of CuO NPs on zebrafish embryos using different parameters including molecular and morphologic. For this purpose, zebrafish embryos at 4 h after post fertilization (hpf) were exposed to different concentrations of CuO NPs (0.5, 1, 1.5 mg/L) until 96 hpf. Mortality, hatching, heartbeat, malformation rates were examined during the exposure period. In addition, Raman spectroscopy was used to determine whether CuO NPs entered into the tissues of zebrafish larvae or not. Moreover, the alterations in the expression of genes related to the antioxidant system and innate immune system were examined in the embryos exposed to CuO NPs during 96 h. The results showed that CuO NPs was not able to enter into the zebrafish embryos/larvae tissues but caused an increased the mortality rate, a delayed hatching, and a decreased heartbeat rate. Moreover, CuO NPs caused several types of abnormalities such as head and tail malformations, vertebral deformities, yolk sac edema, and pericardial edema. RT-PCR results showed that the transcription of mtf-1, hsp70, nfkb and il-1β, tlr-4, tlr-22, trf, cebp was changed by the application of CuO NPs. In conclusion, short-term exposure to CuO NPs has toxic effects on the development of zebrafish embryos.

Aksakal FI ，Ciltas A 《COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY》

Embryotoxicity of nitrophenols to the early life stages of zebrafish (Danio rerio).

The nitrophenols (NPs) are water-soluble compounds. These compounds pose a significant health threat since they are priority environmental pollutants. In this study, 2-Nitrophenol (2NP) and 2,4-dinitrophenol (DNP) were examined for embryo and early life stage toxicity in zebrafish (Danio rerio). Acute toxicity and teratogenicity of 2NP and DNP were tested for 4 days using zebrafish embryos. The typical lesions observed were no somite formation, incomplete eye and head development, tail curvature, weak pigmentation (≤48 hours postfertilization (hpf)), kyphosis, scoliosis, yolk sac deformity, and nonpigmentation (72 hpf). Also, embryo and larval mortality increased and hatching success decreased. The severity of abnormalities and mortalities were concentration- and compound-dependent. Of the compounds tested, 2,4-DNP was found to be highly toxic to the fish embryos following exposure. The median lethal concentrations and median effective concentrations for 2NP are 18.7 mg/L and 7.9 mg/L, respectively; the corresponding values for DNP are 9.65 mg/L and 3.05 mg/L for 48 h. The chorda deformity was the most sensitive endpoint measured. It is suggested that the embryotoxicity may be mediated by an oxidative phosphorylation uncoupling mechanism. This article is the first to describe the teratogenicity and embryotoxicity of two NPs to the early life stages of zebrafish.

Ceylan Z ，Şişman T ，Yazıcı Z ，Altıkat AÖ ... -  《-》

Developmental neurotoxicity of maneb: Notochord defects, mitochondrial dysfunction and hypoactivity in zebrafish (Danio rerio) embryos and larvae.

Broad applications and exposure to the fungicide maneb can lead to toxicity in non-target organisms. Maneb is also associated with neurogenerative diseases such as Parkinson's disease (PD). The objectives of this study were to determine the acute toxicity of maneb to zebrafish by measuring mitochondrial bioenergetics, locomotor activity, and the expression of genes related to the oxidative damage response, as well as those related to dopamine signaling due to its association with PD. Zebrafish embryos at 6 h post-fertilization (hpf) were exposed to either solvent control (0.1% DMSO, v/v), or one dose of 0.1, 0.5, 1.0 and 10.0 µM maneb for 96 h. Maneb was moderately toxic to zebrafish embryos, and had a 96-h LC50 value of 4.29 μM (~ 1.14 mg/L). Maneb induced a dose-dependent increase in mortality, decreased hatching rate, and increased notochord deformity rate at both 1.0 and 10.0 µM after 72 and 96 h. Total body length was also significantly reduced with 1.0 µM maneb. A 50-60% decrease in mean basal oxygen consumption rate was also observed in embryos following a 24 hpf exposure to 10.0 µM maneb but oligomycin-induced ATP production and FCCP-induced maximum respiration remained unaffected. No change was detected in the expression levels of genes associated with oxidative stress (sod1 and sod2), nor those related to dopamine synthesis (th1), dopamine transporter (dat), dopamine receptors (drd1, drd2a, drd3, and drd4b). Thus, modifying the expression of these transcripts may not be a mechanism for maneb-induced developmental toxicity in zebrafish. To assess the potential for neurotoxicity, a dark photokinesis assay was conducted in larvae following 7 d exposure to 0.1, 0.5 and 1.0 μM maneb. Larvae exposed to 0.5 and 1.0 μM maneb showed signs related to hypoactivity, and this reduced activity is hypothesized to be associated with notochord defects as this deformity was prevalent at higher concentrations of maneb. Overall, these data demonstrate that maneb negatively affects embryonic development (i.e. notochord development), affects basal oxygen consumption rates of embryos, and induces hypoactivity in larval fish. This study improves understanding regarding the developmental neurotoxicity of the fungicide maneb to zebrafish.

Cao F ，Souders CL 2nd ，Li P ，Pang S ，Liang X ，Qiu L ，Martyniuk CJ ... -  《-》

Toxic effects of magnesium oxide nanoparticles on early developmental and larval stages of zebrafish (Danio rerio).

Magnesium oxide nanoparticles (MgONPs) are used in medicine, manufacturing and food industries. Because of their extensive application in our daily lives, environmental exposure to these nanoparticles is inevitable. The present study examined the effects of MgONPs on zebrafish (Danio rerio) early developmental stages. The results showed that, at different concentrations, MgONPs induced cellular apoptosis and intracellular reactive oxygen species. The hatching rate and survival of embryos decreased in a dose dependent manner. The 96-h LC50 value of MgONPs on zebrafish survival was 428 mg/l and the 48-h EC50 value of MgONPs on zebrafish embryo hatching rate was 175 mg/l. Moreover different types of malformation were observed in exposed embryos. The results demonstrate the toxic effects of MgONPs on zebrafish embryos and emphasize the need for further studies.

Ghobadian M ，Nabiuni M ，Parivar K ，Fathi M ，Pazooki J ... -  《-》