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Triflumizole Induces Developmental Toxicity, Liver Damage, Oxidative Stress, Heat Shock Response, Inflammation, and Lipid Synthesis in Zebrafish.

ABSTRACT: Triflumizole (TFZ) toxicity must be investigated in the aquatic environment to understand the potential risks to aquatic species. Accordingly, the adverse effects of TFZ exposure in zebrafish were investigated. Results demonstrate that, after TFZ exposure, the lethal concentration 50 (LC₅₀) in 3 d post-fertilization (dpf) embryos and 6 dpf larvae were 4.872 and 2.580 mg/L, respectively. The development (including pericardium edema, yolk sac retention, and liver degeneration) was apparently affected in 3 dpf embryos. Furthermore, the alanine aminotransferase (ALT) activity, superoxide dismutase (SOD) activity, catalase (CAT) activity, and malondialdehyde (MDA) content in 6 dpf larvae were significantly increased. Additionally, the expression of heat shock response genes (including hsp70, grp78, hsp90, and grp94), inflammatory genes (including p65-nfκb, il-1β, and cox2a), and lipid synthetic genes (including srebp1, fas, acc, and ppar-γ) in 3 dpf embryos was significantly increased, which was also partially observed in the intestinal cell line form Pampus argenteus. Taken together, TFZ could affect the development of zebrafish, accompanied by disturbances of oxidative stress, heat shock response, inflammation, and lipid synthesis. Our findings provide an original insight into the potential risks of TFZ to the aquatic ecosystem.

SUBMITTER: Bai L

PROVIDER: S-EPMC9699234 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature

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Triflumizole Induces Developmental Toxicity, Liver Damage, Oxidative Stress, Heat Shock Response, Inflammation, and Lipid Synthesis in Zebrafish.

Bai Lina L Shi Peng P Jia Kun K Yin Hua H Xu Jilin J Yan Xiaojun X Liao Kai K

Toxics 20221117 11

Triflumizole (TFZ) toxicity must be investigated in the aquatic environment to understand the potential risks to aquatic species. Accordingly, the adverse effects of TFZ exposure in zebrafish were investigated. Results demonstrate that, after TFZ exposure, the lethal concentration 50 (LC<sub>50</sub>) in 3 d post-fertilization (dpf) embryos and 6 dpf larvae were 4.872 and 2.580 mg/L, respectively. The development (including pericardium edema, yolk sac retention, and liver degeneration) was appar ...[more]

PMID: 36422906

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Project description:Objective: Epidemiological studies have found air pollution to be a driver of adverse pregnancy outcomes, including gestational diabetes, low term birth weight and preeclampsia. It is unknown what biological mechanisms are involved in this process. A first trimester trophoblast cell line (HTR-8/SVneo) was exposed to various concentrations of PM2.5 (PM2.5) in order to elucidate the effect of urban particulate matter (PM) of size <2.5 μm on placental function. Methods: PM2.5 were collected at a site representative of urban traffic and dispersed in cell media by indirect and direct sonication. The HTR-8 cells were grown under standard conditions. Cellular uptake was studied after 24 and 48 h of exposure by transmission electron microscopy (TEM). The secretion of human chorionic gonadotropin (hCG), progesterone, and Interleukin-6 (IL-6) was measured by ELISA. Changes in membrane integrity and H2O2 production were analyzed using the CellToxTM Green Cytotoxicity and ROSGloTM assays. Protease activity was evaluated by MitoToxTM assay. Mitochondrial function was assessed through high resolution respirometry in an Oroboros O2k-FluoRespirometer, and mitochondrial content was quantified by citrate synthase activity. Results: TEM analysis depicted PM2.5 cellular uptake and localization of the PM2.5 to the mitochondria after 24 h. The cells showed aggregated cytoskeleton and generalized necrotic appearance, such as chromatin condensation, organelle swelling and signs of lost membrane integrity. The mitochondria displayed vacuolization and disruption of cristae morphology. At 48 h exposure, a significant drop in hCG secretion and a significant increase in progesterone secretion and IL-6 production occurred. At 48 h exposure, a five-fold increase in protease activity and a significant alteration of H2O2 production was observed. The HTR-8 cells exhibited evidence of increased cytotoxicity with increasing exposure time and dose of PM2.5. No significant difference in mitochondrial respiration or mitochondrial mass could be demonstrated. Conclusion: Following exposure to air pollution, intracellular accumulation of PM may contribute to the placental dysfunction associated with pregnancy outcomes, such as preeclampsia and intrauterine growth restriction, through their direct and indirect effects on trophoblast protein secretion, hormone regulation, inflammatory response, and mitochondrial interference.

Dataset Information

Triflumizole Induces Developmental Toxicity, Liver Damage, Oxidative Stress, Heat Shock Response, Inflammation, and Lipid Synthesis in Zebrafish.

Publications

Triflumizole Induces Developmental Toxicity, Liver Damage, Oxidative Stress, Heat Shock Response, Inflammation, and Lipid Synthesis in Zebrafish.

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