[en] In the past few decades, extensive application of azoxystrobin has led to great concern regarding its adverse effects on aquatic organisms. The objective of the present study was to evaluate the reproductive toxicity of azoxystrobin to zebrafish. After adult zebrafish of both sexes were exposed to 2, 20 and 200 μg/L azoxystrobin for 21 days, egg production, the fertilization rate, the gonadosomatic index (GSI) and hepatosomatic index (HSI), 17β-estradiol (E2), testosterone (T) and vitellogenin (Vtg) concentrations, and histological alterations in the gonads and livers were measured. Meanwhile, expression alterations of genes encoding gonadotropins and gonadotropin receptors (fshb, lhb, fshr and lhr), steroid hormone receptors (era, er2b and ar), steroidogenic enzymes (cyp11a, cyp11b, cyp17, cyp19a, cyp19b, hsd3b and hsd17b) in the hypothalamic-pituitary-gonad (HPG) axis and vitellogenin (vtg1 and vtg2) in the livers were also investigated. The results showed that reduced egg production and fertilization rates were observed at 200 μg/L azoxystrobin. In female zebrafish, reduced E2 and Vtg concentrations, decreased GSI, increased T concentrations, and histological alterations in the ovaries and livers were observed at 200 μg/L azoxystrobin, along with significant down-regulation of lhb, cyp19b, lhr, cyp19a, vtg1 and vtg2, and up-regulation of cyp17, hsd3b and hsd17b. In male zebrafish, increased E2 and Vtg concentrations, reduced T concentration and GSI, and histological alterations in the testes and livers were observed after exposure to 20 and 200 μg/L azoxystrobin, along with significant up-regulations of cyp19b, cyp11a, cyp17, cyp19a, hsd3b and hsd17b, vtg1 and vtg2. Moreover, cyp11a, hsd3b, cyp19a, vtg1 and vtg2 in male zebrafish were significantly up-regulated after treatment with 2 μg/L azoxystrobin. The results of the present study indicate that azoxystrobin led to reproductive toxicity in zebrafish and male zebrafish were more sensitive to azoxystrobin than female zebrafish. - Highlights: • Azoxystrobin reduced egg production and the fertilization rate of adult zebrafish. • The sex steroid hormones and Vtg concentrations were altered by azoxystrobin. • Gonadal and hepatic pathology in zebrafish was induced by azoxystrobin. • Azoxystrobin induced expression alteration of genes in the HPG axis and livers. • Male zebrafish were more sensitive to azoxystrobin than female zebrafish. - Azoxystrobin induced adverse effects on zebrafish reproduction and male zebrafish were more sensitive to azoxystrobin than female zebrafish.

[en] Cyhalofop-butyl is a selective herbicide widely employed in paddy field, which can transfer into aquatic environments. However, details of the environmental risk and aquatic toxicity of cyhalofop-butyl have not been fully investigated. In this study, zebrafish (Danio rerio) embryos were exposed to a range of cyhalofop-butyl until 120 hour post-fertilization (hpf) to assess embryonic toxicity of the chemical. Our results demonstrated that cyhalofop-butyl was highly toxic to zebrafish embryos, with concentration-dependent negative effects in embryonic development. In addition, exposure to cyhalofop-butyl resulted in significant increases in reactive oxygen species (ROS) production and cell apoptosis in heart area. The mRNA levels of the genes related to oxidative stress and apoptosis were also altered significantly after cyhalofop-butyl exposure. Moreover, the activity of capspase-9 and caspase-3 were significantly increased. Therefore, we speculated that oxidative stress-induced apoptosis should be responsible for abnormal development during embryogenesis after cyhalofop-butyl exposure. - Highlights: • Cyhalofop-butyl can induce developmental toxicity in zebrafish embryos. • Cyhalofop-butyl can induce oxidative stress and apoptosis in zebrafish embryos. • Oxidative stress-induced apoptosis might be responsible for abnormal development. - Cyhalofop-butyl could induce negative effects in embryonic development. The cyhalofop-butyl – induced developmental toxicity could be explained by oxidative stress-induced apoptosis

[en] Propiconazole (PCZ) is a widely used fungicide around the world and was frequently detected in surface waters, which would pose risk to aquatic organisms. Previous studies indicated that PCZ has high toxicity to different kinds of fish. However, most of the studies focus on the toxicity and mechanisms of PCZ to adult fish, the potential toxicity mechanism of PCZ to fish embryos is still poorly understood. The present study investigated the effects of PCZ on content of reactive oxygen species (ROS) and malondialdehyde (MDA); activities of superoxide dismutase (SOD), catalase (CAT), and Na⁺-K⁺-ATPase; and expression level of genes related to oxidative stress, cell apoptosis, and innate immune system in zebrafish embryos after 96-h exposure. The results showed that 5.0 mg/L PCZ induced oxidative damage in zebrafish embryos, as indicated by increased ROS and MDA content and alteration of antioxidative enzyme activity. The activity of Na⁺-K⁺-ATPase in zebrafish embryos was significantly inhibited after exposure to 0.5 mg/L PCZ. The expression levels of bax, p53, casp-3, casp-9, and apaf-1 were significantly increased, indicating that cell apoptosis was caused in embryos by 5.0 mg/L PCZ. The expression level of interleukin-1b (IL-1b) and IL-8 increased after exposure to 0.5 mg/L PCZ, but that of IL-1b, IL-8, and cxcl-c1c (chemokine (C-X-C motif) ligand 18b) decreased in 5.0-mg/L PCZ treatment group, indicating an immunotoxicity effect. Our results suggest that oxidative damage, cell apoptosis, and immunotoxicity would be induced in zebrafish embryos after short-term exposure to PCZ.

[en] Highlights: • Sublethal concentration of metamifop induced hepatic inflammation in adult zebrafish. • Metamifop caused lipid accumulation in adult zebrafish liver. • Metamifop induced cholesterol metabolism disorder in adult zebrafish liver. • Metamifop elevated the abundance of 91 lipids that mainly belong to triglyceride lipid class. Metamifop (MET) is an effective herbicide that has been extensively used in paddy fields. Previous research demonstrated that MET was highly toxic to zebrafish embryos, and this threat has caused great concern; moreover, 0.40 mg/L MET elevated the hepatosomatic index (HSI) in adult zebrafish without lethal effect after 21 d of exposure. In this study, we further determined the detailed impacts of MET on adult zebrafish at sublethal concentrations (0.025, 0.10 and 0.40 mg/L). We found that 0.40 mg/L MET caused liver injury by increasing the activity of aspartate aminotransferase and alanine aminotransferase in plasma, the content of interleukin-1β, IL-6, tumor necrosis factor-α, and mRNA expression level of genes associated with inflammatory response in liver of adult zebrafish. The hepatic triglyceride (TG), free fatty acid and fatty acid synthase levels were significantly elevated in 0.40 mg/L MET-treated group (1.55-, 2.20- and 2.30-fold, respectively), and the transcript of lipid accumulation-related genes (fabp10, fas, acc, chrebp, dagt2 and agpat4) were upregulated. Meanwhile, the total cholesterol content was decreased by 0.48-fold, bile acid level was increased by 2.44-fold, and levels of cholesterol metabolism-related genes (apoa-1a, hmgcra, cyp51, dhcr7 and cyp7a1) were increased, suggesting cholesterol metabolism disorder occurred in zebrafish. Furthermore, analysis of lipidomics revealed that 0.40 mg/L MET significantly increased the abundance of 91 lipids, which mainly belonged to TG lipid class and were enriched in pathways of glycerolipid metabolism, cholesterol metabolism, etc. These results suggested that MET exposure at sublethal concentrations would induce hepatic inflammation and lipid metabolism disorders in adult zebrafish.