Difenoconazole causes spleen tissue damage and immune dysfunction of carp through oxidative stress and apoptosis

Ecotoxicology and Environmental Safety, Год журнала: 2022, Номер 237, С. 113563 - 113563

Опубликована: Апрель 26, 2022

As the use of pesticides increases year after year, so does level residual in aquatic environment, posing a serious threat to non-target organisms. Difenoconazole (DFZ), class long-lasting fungicides and residues marine has been shown cause damaging effects on different organs However, there is no research damage DFZ carp spleen tissue. This study aimed investigate acute toxic tissue (Cyprinus carpio) by exposing juvenile environmentally relevant concentrations DFZ. We randomly selected 30 carp, divided them into Control, Low, High groups, then exposed three groups 0, 0.488 mg/L DFZ, 1.953 for 96 h respectively. investigated caused tissues detecting changes histopathologic damage, apoptosis, oxidative stress, inflammation, blood biochemical parameters. found that causes severe histopathology tissue, including ballooning, structural relaxation, giant mitochondria. In addition, we excessive apoptosis TUNEL staining expression levels apoptosis-related genes (caspase3, caspase8, caspase9, fas, bax, bcl-2, p53). The activities transcript antioxidant enzymes SOD, CAT, GSH-Px were significantly down-regulated. led significant increase activation NF-κB signaling pathway mRNA pro-inflammatory cytokines il-6, il-1β, tnf-α, substantial decrease anti-inflammatory il-10 tgf-β1 Blood parameters showed exposure reduced erythrocyte, leukocyte, hemoglobin, C3, IgM levels. Collectively, induced immunosuppression, inflammatory responses resulting damage.

Язык: Английский

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Induction of developmental toxicity and cardiotoxicity in zebrafish embryos by Emamectin benzoate through oxidative stress

The Science of The Total Environment, Год журнала: 2022, Номер 825, С. 154040 - 154040

Опубликована: Фев. 20, 2022

Язык: Английский

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Difenoconazole causes cardiotoxicity in common carp (Cyprinus carpio): Involvement of oxidative stress, inflammation, apoptosis and autophagy

Chemosphere, Год журнала: 2022, Номер 306, С. 135562 - 135562

Опубликована: Июль 2, 2022

Язык: Английский

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Toxicity analysis of endocrine disrupting pesticides on non-target organisms: A critical analysis on toxicity mechanisms

Toxicology and Applied Pharmacology, Год журнала: 2023, Номер 474, С. 116623 - 116623

Опубликована: Июль 4, 2023

Язык: Английский

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Emerging disinfection byproducts 3-bromine carbazole induces cardiac developmental toxicity via aryl hydrocarbon receptor activation in zebrafish larvae

Environmental Pollution, Год журнала: 2024, Номер 346, С. 123609 - 123609

Опубликована: Фев. 23, 2024

Язык: Английский

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Vitamin A ameliorates valproic acid-induced autism-like symptoms in developing zebrafish larvae by attenuating oxidative stress and apoptosis

NeuroToxicology, Год журнала: 2024, Номер 101, С. 93 - 101

Опубликована: Янв. 6, 2024

Язык: Английский

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Effects of Difenoconazole on Tubifex tubifex: Antioxidant Activity, Insights from GUTS Predictions, and Multi-Biomarker Analysis

Biology, Год журнала: 2025, Номер 14(3), С. 302 - 302

Опубликована: Март 17, 2025

The increasing demand for agricultural products has led to a rise in pesticide use, resulting the pollution of aquatic habitats and raising significant health concerns both life humans. Difenoconazole, triazole fungicide, is becoming increasingly popular agriculture, yet its effects on non-target organisms, such as annelids, are not well understood. This study aimed investigate toxicological difenoconazole assess potential impact toxicity biomarkers, using Tubifex tubifex model organism, better understand ecotoxicity freshwater annelids. 96-h LC50 value was determined be 2.68 mg/L. Sublethal concentrations (10% 20% value; 0.268 0.536 mg/L, respectively) caused changes activities oxidative stress enzymes. A concentration- time-dependent decrease superoxide dismutase (SOD), catalase (CAT), glutathione transferase (GST) observed compared control organisms. Additionally, malondialdehyde (MDA) increased throughout exposure period. An Integrated Biomarker Response (IBR) assessment used characterize illustrate T. tubifex. In conclusion, this fungicide appears reduce survival rate at acute levels disrupt normal behavioral patterns. Moreover, it alters enzyme during sublethal exposure. Long-term could potentially have population-level consequences, including reduction number individuals within population.

Язык: Английский

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Difenoconazole disrupts the blood-brain barrier and results in neurotoxicity in carp by inhibiting the Nrf2 pathway mediated ROS accumulation

Ecotoxicology and Environmental Safety, Год журнала: 2022, Номер 244, С. 114081 - 114081

Опубликована: Сен. 13, 2022

Excessive use of hard-to-degrade pesticides threatens the ecological health aquatic systems. This study aimed to investigate difenoconazole (DFZ) residues in environment induced neurotoxicity carp and underlying mechanisms. A total thirty-six carps were divided into three groups exposed 0, 0.5, 2.0 mg/L DFZ for 96 h, respectively. The alterations behavior blood-brain barrier (BBB) examined, potential mechanisms explored using immunological assays biochemical methods. results showed that exposure caused behavioral freezing, reduced feeding, neuronal necrosis carp. Mechanistically, triggered ROS accumulation destroyed balance between oxidation antioxidation with increased lipid peroxidation product MDA contents antioxidant enzymes SOD CAT activities brain by inhibiting NF-E2-related factor 2 (Nrf2) pathway. activation oxidative stress further tight junction proteins MMP levels, thereby destroying BBB leading leakage brain. Increased permeability additionally led nuclear kappa-B signaling-mediated inflammatory cytokine storm, exacerbating neuroinflammation. Meanwhile, activated mitochondria-associated apoptosis carp's up-regulating Bcl-2 associated X protein, cleaved-caspase3, cytochrome C decreasing B-cell lymphoma-2 levels. Interestingly, initiated a protective autophagic response via PI3K/AKT/TOR pathway intending counteract DFZ. Overall, we concluded at high concentrations systems disrupted resulted through inhibition Nrf2 pathway-mediated accumulation. provides reference monitoring new target treatment DFZ-induced

Язык: Английский

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Nano-TiO2 aggravates bioaccumulation and developmental neurotoxicity of difenoconazole in zebrafish larvae via oxidative stress and apoptosis: Protective role of vitamin C

Ecotoxicology and Environmental Safety, Год журнала: 2023, Номер 251, С. 114554 - 114554

Опубликована: Янв. 20, 2023

Titanium dioxide nanoparticles (n-TiO2) could enhance the bioavailability and toxicity of coexisting organic contaminants in aquatic environment. This study attempted to investigate combined effects n-TiO2 difenoconazole (DIF) on neurodevelopment zebrafish underlying mechanisms. In this study, embryos were exposed (100 μg/L), DIF (0, 0.1 0.5 mg/L) their mixtures from 4 96 h post fertilization (hpf) neurotoxicity was evaluated. Our results indicated that adsorbed into brain significantly enhanced bioaccumulation mg/L co-exposure group. 100 μg/L not developmentally toxic larvae, but it exacerbated DIF-induced neurobehavioral alterations larvae. also aggravated suppression central nervous system (CNS) neurogenesis Tg (HuC:egfp) zebrafish, motor neuron axon length (hb9:egfp) downregulation neurodevelopmental genes (elavl3, ngn1, gap43, gfap mbp). addition, elevated oxidative stress by accumulation reactive oxygen species (ROS) inhibition antioxidant enzymes, triggered apoptosis upregulation p53, bax, bcl-2 caspase-3, which markedly intensified presence n-TiO2. Moreover, vitamin C (VC) ameliorated n-TiO2/DIF-induced abnormal locomotor behaviors inhibiting apoptosis, indicating are involved neurotoxicity. Taken together, our data heightened thereby inducing exemplifies importance assessment chemical novel insights mitigate toxicity.

Язык: Английский

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Developmental Neurotoxicity of Difenoconazole in Zebrafish Embryos

Toxics, Год журнала: 2023, Номер 11(4), С. 353 - 353

Опубликована: Апрель 8, 2023

Difenoconazole is a type of triazole fungicide that widely used in the treatment plant diseases. Triazole fungicides have been shown several studies to impair development nervous system zebrafish embryos. There still little known about difenoconazole-induced neurotoxicity fish. In this study, embryos were exposed 0.25, 0.5, and 1 mg/L difenoconazole solution until 120 h post-fertilization (hpf). The difenoconazole-exposed groups showed concentration-dependent inhibitory tendencies heart rate body length. Malformation spontaneous movement increased, locomotor activity decreased highest exposure group. content dopamine acetylcholine was reduced significantly groups. acetylcholinesterase (AChE) also increased after with difenoconazole. Furthermore, expression genes involved neurodevelopment remarkably altered, which corresponded alterations neurotransmitter AChE activity. These results indicated might affect through influencing levels, enzyme activity, neural-related genes, ultimately leading abnormal early stages zebrafish.

Язык: Английский

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