Jinhua Jiang

Embryonic exposure to carbendazim induces the transcription of genes related to apoptosis, immunotoxicity and endocrine disruption in zebrafish (Danio rerio)

Carbendazim is one of the most widespread environmental contaminant that can cause major concern to human and animal reproductive system. To date, very few studies have been conducted on the toxic effect of carbendazim in the non-target organism zebrafish (Danio rerio). The study presented here aimed to assess how carbendazim triggers apoptosis, immunotoxicity and endocrine disruption pathways in zebrafish during its embryo development. Our results demonstrated that the expression patterns of many key genes involved in cell apoptosis pathway (e.g. P53, Mdm2, Bbc3 and Cas8) were significantly up-regulated upon the exposure to carbendazim at the concentration of 500 μg/L, while the Bcl2 and Cas3 were down-regulated at the same concentration, interestingly, the expression level of Ogg1 decreased at all the exposure concentrations. It was also observed that the mRNA levels of CXCL-C1C, CCL1, IL-1b and TNFα which were closely related to the innate immune system, were affected in newly hatched zebrafish after exposed to different concentrations of carbendazim. Moreover, the expression of genes that are involved in the hypothalamic-pituitary-gonadal/thyroid (HPG/HPT) axis including VTG, ERα, ERβ2, Dio1, Dio2, Thraa and Thrb were all down-regulated significantly after the exposure to carbendazim. The expression levels of two cytochrome P450 aromatases CYP19a and CYP19b were increased significantly after 20 and 100 μg/L carbendazim exposure, respectively. Taken together, our results indicated that carbendazim had the potential to induce cell apoptosis and cause immune toxicity as well as endocrine disruption in zebrafish during the embryo developmental stage. The information presented here also help to elucidate the environmental risks caused by the carbendazim-induced toxicity in aquatic organisms.

Effect of acetochlor on transcription of genes associated with oxidative stress, apoptosis, immunotoxicity and endocrine disruption in the early life stage of zebrafish

The study presented here aimed to characterize the effects of acetochlor on expression of genes related to endocrine disruption, oxidative stress, apoptosis and immune system in zebrafish during its embryo development. Different trends in gene expression were observed after exposure to 50, 100, 200μg/L acetochlor for 96h. Results demonstrated that the transcription patterns of many key genes involved in the hypothalamic-pituitary-gonadal/thyroid (HPG/HPT) axis (e.g., VTG1, ERβ1, CYP19a and TRα), cell apoptosis pathway (e.g., Bcl2, Bax, P53 and Cas8), as well as innate immunity (e.g., CXCL-C1C, IL-1β and TNFα) were affected in newly hatched zebrafish after exposure to acetochlor. In addition, the up-regulation of CAT, GPX, GPX1a, Cu/Zn-SOD and Ogg1 suggested acetochlor might trigger oxidative stress in zebrafish. These finding indicated that acetochlor could simultaneously induce multiple responses during zebrafish embryonic development, and bidirectional interactions among oxidative stress, apoptosis pathway, immune and endocrine systems might be present.

Susceptibility to selected insecticides and risk assessment in the insect egg parasitoid Trichogramma confusum (Hymenoptera: Trichogrammatidae).

ABSTRACT The parasitoid Trichogramma confusum Viggiani (Hymenoptera: Trichogrammatidae) is an important natural enemy of many lepidopterans throughout the world. Extensive toxicological tests have clarified the toxic effects of insecticides on trichogrammatids, but only few studies have examined these effects on T. confusum. Among the seven classes of tested chemicals, organophosphates and carbamates exhibited the highest intrinsic toxicity to the parasitoid with LC50 values ranging from 0.037 (0.030–0.046) to 0.29 (0.23–0.38) and from 0.17 (0.15–0.19) to 1.61 (1.45–1.79) mg AI L-1, respectively. They were followed by phenylpyrazoles, avermectins, pyrethroids, and neonicotinoids, which induced variable toxicity responses with LC50 values ranging from 0.63 to 45.26, 1.06–21.73, 3.89–19.36, and 0.24–754.2 mg AI L-1, respectively. In contrast, insect growth regulators (IGRs) showed the least toxicity to the parasitoid with LC50 values ranging from 3,907 (3,432–4,531 ) to 10,154 (8,857–12,143) mg AI L-1. A risk quotient analysis indicated that neonicotinoids (except thiamethoxam), avermectins, pyrethroids, IGRs, and phenylpyrazoles are safe, but organophosphates and carbamates are slightly to moderately or dangerously toxic to T. confusum. This study provides informative data for implementing both biological and chemical control strategies in integrated pest management of lepidopterans.

Pretilachlor has the potential to induce endocrine disruption, oxidative stress, apoptosis and immunotoxicity during zebrafish embryo development

The objectives of the present study were to investigate the toxic effects of pretilachlor on zebrafish during its embryo development. The results demonstrated that the transcription of genes involved in the hypothalamic-pituitary-gonadal/thyroid (HPG/HPT) axis was increased after exposure to 50, 100, 200 μg/L pretilachlor for 96 h, the aromatase activity, vitellogenin (VTG) and thyroid hormones T3 and T4 levels in zebrafish were also up-regulated simultaneously. Pretilachlor exposure induced a noticeable increase in ROS level, increased the transcription and level of antioxidant proteins (e.g., CAT, SOD and GPX). Moreover, the up-regulation of P53, Mdm2, Bbc3 expression and Caspase3 and Caspase9 activities in the apoptosis pathway suggested pretilachlor might trigger cell apoptosis in zebrafish. In addition, the transcription of CXCL-C1C, IL-1β and IL-8 related to the innate immunity was down-regulated after pretilachlor exposure. These data suggested that pretilachlor could simultaneously induce endocrine disruption, apoptosis, oxidative stress and immunotoxicity during zebrafish embryo development.

Carbendazim has the potential to induce oxidative stress, apoptosis, immunotoxicity and endocrine disruption during zebrafish larvae development.

Increasing evidence have suggested deleterious effects of carbendazim on reproduction, apoptosis, immunotoxicity and endocrine disruption in mice and rats, however, the developmental toxicity of carbendazim to aquatic organisms remains obscure. In the present study, we utilized zebrafish as an environmental monitoring model to characterize the effects of carbendazim on expression of genes related to oxidative stress, apoptosis, immunotoxicity and endocrine disruption during larval development. Different trends in gene expression were observed upon exposing the larvae to 4, 20, 100, and 500 μg/L carbendazim for 4 and 8d. The mRNA levels of catalase, glutathione peroxidase and manganese superoxide dismutase (CAT, GPX, and Mn/SOD) were up-regulated after exposure to different concentrations of carbendazim for 4 or 8d. The up-regulation of p53, Apaf1, Cas8 and the down-regulation of Bcl2, Mdm2, Cas3 in the apoptosis pathway, as well as the increased expression of cytokines and chemokines, including CXCL-C1C, CCL1, IL-1b, IFN, IL-8, and TNFα, suggested carbendazim might trigger apoptosis and immune response during zebrafish larval development. In addition, the alteration of mRNA expression of VTG, ERα, ERβ1, ERβ2, TRα, TRβ, Dio1, and Dio2 indicated the potential of carbendazim to induce endocrine disruption in zebrafish larvae. These data suggested that carbendazim could simultaneously induce multiple responses during zebrafish larval development, and bidirectional interactions among oxidative stress, apoptosis pathway, immune and endocrine systems might be present.

Potential Dermal Exposure and Risk Assessment for Applicators of Chlorothalonil and Chlorpyrifos in Cucumber Greenhouses in China

ABSTRACT Occupational exposure to pesticides has not been conducted in depth so far in China. The potential dermal exposure and risk assessment were conducted for applicators through application with a knapsack power sprayer in cucumber greenhouses. The spray suspension was prepared with 75% chlorothalonil WP and 48% chlorpyrifos EC. The dermal patch method was applied to assess the potential dermal exposure (PDE) of applicators during application. The average total PDE on the whole body of applicators during application of chlorothalonil and chlorpyrifos was 83.2 mL h−1 and 85.1 mL h−1, respectively. The most exposed part of the body was arms, especially the right arm. For risk assessment, the margin of safety (MOS) was calculated from the PDE. The MOS values were 0.1 and 0.2 for application of chlorothalonil and chlorpyrifos, respectively, both less than 1, which indicated low possibility of health risk.

Individual and combined toxic effects of herbicide atrazine and three insecticides on the earthworm, Eisenia fetida

In the present study, we evaluated the individual and combined toxic effects of herbicide atrazine and three insecticides (chlorpyrifos, lambda-cyhalothrin and imidacloprid) on the earthworm, Eisenia fetida. Results from 48-h filter paper test indicated that imidacloprid had the highest toxicity to E. fetida with an LC50 of 0.05 (0.041–0.058) μg a.i. cm−2, followed by lambda-cyhalothrin and atrazine with LC50 values ranging from 4.89 (3.52–6.38) to 4.93 (3.76–6.35) μg a.i. cm−2, while chlorpyrifos had the least toxicity to the worms with an LC50 of 31.18 (16.22–52.85) μg a.i. cm−2. Results from 14-days soil toxicity test showed a different pattern of toxicity except that imidacloprid was the most toxic even under the soil toxicity bioassay system. The acute toxicity of atrazine was significantly higher than that of chlorpyrifos. In contrast, lambda-cyhalothrin was the least toxic to the animals under the soil toxicity bioassay system. The binary mixture of atrazine–lambda-cyhalothrin and ternary mixture of atrazine–chlorpyrifos–lambda-cyhalothrin displayed a significant synergistic effect on the earthworms under the soil toxicity bioassay. Our findings would help regulatory authorities understand the complexity of effects from pesticide mixtures on non-target organisms and provide useful information of the interaction of various pesticide classes detected in natural environment.

Biological response of zebrafish after short-term exposure to azoxystrobin

Azoxystrobin (AZ) is a broad-spectrum systemic fungicide that widely used in the world. The present study investigated the toxicity effects on zebrafish after short-term exposure of AZ. Results demonstrated that the larval stage was most susceptible to AZ in the multiple life stages of zebrafish, with 96 h-LC50 value of 0.777 mg/L. Zebrafish larvae were exposed to different AZ concentrations (0, 0.1, 1, 10, 100 μg/L) and examined on 24, 48 and 72 h. It was found that AZ induced ROS accumulation, increased GST, GPX and POD activity and the transcriptions of antioxidant and stress response related genes, while the opposite trend occurred for SOD and CAT activity in 24-h or 48-h exposure period. The increased E2 and VTG levels in zebrafish larvae, and altered transcription levels of regulatory and steroidogenic genes in the hypothalamus-pituitary-gonad (HPG) axis indicated the endocrine disruption capacity of AZ. The transcripts of mdm2, p53, ogg1, bcl2, bbc3, cas8 and cas9 involved in cell apoptosis, and the mRNA levels of cytokines and chemokines such as cxcl-c1c, ccl, il-1β, il-8, ifn, and tnfα were in accordance with the trends of the examined genes involved in oxidative stress and endocrine system. The results suggested that short-term exposure to AZ might impose ecotoxicological effects on zebrafish larvae, and the information presented here also provide molecular strategies and increase mechanistic understanding of AZ-induced toxic response, and help elucidate the environmental risks of AZ.

Synergistic potential of fenvalerate and triadimefon on endocrine disruption and oxidative stress during rare minnow embryo development

Pyrethroids have been reported to interact synergistically when co‐exposed with azoles fungicides in different organisms. In the present study, we investigated the mixture toxicity of fenvalerate (FEN) and triadimefon (TDF) toward embryos of Gobiocypris rarus after 96 h exposure. Results demonstrated that TDF enhanced the acute toxicity of FEN. Exposure to binary mixtures of FEN and TDF resulted in synergistic responses of endocrine disruption by inducing the transcripts of several genes including vtg, erα, erβ1, erβ2, cyp19a, cyp1a, cyp4, cyp11a, gnrh3, gnrhr1a, star, and dmrt1. Furthermore, FEN and TDF mixture increased the VTG level and aromatase activity in rare minnow embryos. FEN and TDF co‐exposure also regulated the mRNA of vezf, hsp70, p53, gadd45α, induced the synthesis of ROS and activity of GST, suggesting the synergistic potential of oxidative stress induced by FEN and TDF co‐exposure. The results indicated that binary mixtures of FEN and TDF could simultaneously induce endocrine disruption and oxidative stress in a synergistic manner during rare minnow embryo development.