Journal of Environmental Sciences
·
2024
·
IF 5.9
Feixue Liu,Tianmeng Zhang,Yeyun Ma,Jingquan Dong,Yong Sun
Environmental residues of the fungicide difenoconazole (DFZ) have been shown to pose a threat to mammals. However, the risk assessment of DFZ for cultured carp remains unclear. The aim of this study was to investigate the adverse effects of DFZ on carp liver and their molecular mechanisms by simulating the environmental contamination concentrations of DFZ. Our results showed that DFZ induced structural damage in the liver, including edema, vacuolation, and congestion. In addition, DFZ residues were detected in liver tissues. Mechanistically, DFZ causes mitochondrial dysfunction by promoting Ca 2+ transfer from the endoplasmic reticulum (ER) to mitochondria via IP3R, leading to the onset of ROS burst and apoptosis, and the inhibition of Nrf2 antioxidant function by DFZ also results in uncontrolled ROS. Mitophagy was also activated intracellularly to counteract mitochondrial damage. Interestingly, treatment with 2-APB alleviated mitochondrial dysfunction, restored the mitochondrial membrane potential, and inhibited apoptosis by blocking the translocation of Ca 2+ from the ER to the mitochondria. Metabolomic analysis revealed that DFZ disrupted energy metabolism in carp liver, whereas 2-APB reversed DFZ-induced metabolic alterations. In conclusion, the present study elucidates the threat of DFZ to carp liver and highlights the mechanism of damage, thereby helping to explain the impact of agriculture on the aquatic environment.
研究领域:
环境科学
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毒理学
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水生生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2024
·
IF 3.3
Xiaomeng Ji,Jiajia Guo,Yeyun Ma,Shuai Zhang,Zuwang Yang,Yuanyuan Li,Kaixin Ping,Yue Xin,Zibo Dong
Difenoconazole (DFZ) is a fungicidal pesticide extensively employed for the management of fungal diseases in fruits, vegetables, and cereal crops. However, its potential environmental impact cannot be ignored, as DFZ accumulation is able to lead to aquatic environment pollution and harm to non-target organisms. Quercetin (QUE), a flavonoid abundant in fruits and vegetables, possesses antioxidant and anti-inflammatory properties. In this article, carp were exposed to 400 mg/kg QUE and/or 0.3906 mg/L DFZ for 30 d to investigate the effect of QUE on DFZ-induced respiratory toxicity in carp. Research shows that DFZ exposure increases reactive oxygen species (ROS) production in the carp's respiratory system, leading to oxidative stress, inflammation, and damage to gill tissue and tight junction proteins. Further research demonstrates that DFZ induces mitochondrial dynamic imbalance and gill cell apoptosis. Notably, QUE treatment significantly reduces ROS levels, alleviates oxidative stress and inflammation, and mitigates mitochondrial dynamics imbalance and mitochondrial apoptosis. This study emphasizes the profound mechanism of DFZ toxicity to the respiratory system of common carp and the beneficial role of QUE in mitigating DFZ toxicity. These findings contribute to a better understanding of pesticide risk assessment in aquatic systems and provide new insights into strategies to reduce their toxicity.
研究领域:
水生毒理学
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环境科学
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药理学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2023
·
IF 6.8
Renfei Zhu,Chunlan Liu,Jingyu Wang,Li Zou,Fan Yang,Xia Chi,Jiansheng Zhu
Titanium dioxide nanoparticles (n-TiO 2 ) could enhance the bioavailability and toxicity of coexisting organic contaminants in the aquatic environment. This study attempted to investigate the combined effects of n-TiO 2 and difenoconazole (DIF) on the neurodevelopment of zebrafish and the underlying mechanisms. In this study, zebrafish embryos were exposed to n-TiO 2 (100 μg/L), DIF (0, 0.1 and 0.5 mg/L) and their mixtures from 4 to 96 h post fertilization (hpf) and neurotoxicity was evaluated. Our results indicated that n-TiO 2 adsorbed DIF into the brain of zebrafish and significantly enhanced the bioaccumulation of DIF and n-TiO 2 in the 0.5 mg/L co-exposure group. 100 μg/L n-TiO 2 was not developmentally toxic to the zebrafish larvae, but it exacerbated DIF-induced neurobehavioral alterations in the zebrafish larvae. n-TiO 2 also aggravated DIF-induced suppression of central nervous system (CNS) neurogenesis in Tg ( HuC:egfp ) zebrafish, motor neuron axon length in Tg ( hb9:egfp ) zebrafish, and downregulation of neurodevelopmental genes ( elavl3 , ngn1 , gap43 , gfap and mbp ). In addition, DIF elevated oxidative stress by accumulation of reactive oxygen species (ROS) and inhibition of antioxidant enzymes, and triggered apoptosis by upregulation of p53 , bax , bcl-2 and caspase-3 , which were markedly intensified in the presence of n-TiO 2 . Moreover, vitamin C (VC) ameliorated n-TiO 2 /DIF-induced abnormal locomotor behaviors and neurotoxicity by inhibiting oxidative stress and apoptosis, indicating that oxidative stress and apoptosis are involved in n-TiO 2 /DIF-induced neurotoxicity. Taken together, our data indicated that n-TiO 2 enhanced the accumulation of DIF and heightened oxidative stress and apoptosis, thereby inducing neurotoxicity. This study exemplifies the importance of the toxicity assessment of chemical mixtures and novel insights to mitigate their combined toxicity.
研究领域:
环境毒理学
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神经科学
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水生生物学
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药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
·
2024
·Vol. 31
·期 13
·19396-19408
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IF 0
Pan Enzhuang,Xin Yue,Li Xueqing,Ping Kaixin,Li Xing,Sun Ying,Xu Xuhui,Dong Jingquan
As a broad-spectrum and efficient triazole fungicide, difenoconazole is widely used, which not only pollutes the environment but also exerts toxic effects on non-target organisms. The spleen plays an important role in immune protection as an important secondary lymphoid organ in carp. In this study, we assessed the protective impact of silybin as a dietary additive on spleen tissues of carp during exposure to difenoconazole. Sixty carp were separated into four groups for this investigation including control group, difenoconazole group, silybin group, and silybin and difenoconazole group. By hematoxylin-eosin staining, dihydroethidium staining, immunohistochemical staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, quantitative real-time PCR assay, Western blot analysis, biochemical assays, and immune function indicator assays, we found that silybin could prevent difenoconazole-induced spleen tissue damage, oxidative stress, and immune dysfunction, and inhibited apoptosis of carp spleen tissue cells by suppressing the formation of p53-driven caspase-9-apoptotic protease activating factor-1-cytochrome C complex. The results suggested that silybin as a dietary additive could improve spleen tissue damage and immune dysfunction induced by difenoconazole in aquaculture carp.
研究领域:
环境毒理学
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免疫学
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水产养殖学
✓ 已验证
DOI
危险品化学品经营许可证（带存储）