Toxic effects of boscalid in adult zebrafish (Danio rerio) on carbohydrate and lipid metabolism

Qian, Le; Zhang, Jie; Chen, Xiangguang; Qi, Suzhen; Wu, Peizhuo; Wang, Chen; Wang, Chengju

doi:10.1016/j.envpol.2019.01.054

Cited by 56 publications

(20 citation statements)

References 55 publications

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“…The lack of species specificity of the inhibitory effect of SDHIs due to this mechanism of action is indeed known to agrochemical manufacturers, part of the SDHIs were reported to also be efficient against nematodes [39]. Similarly, the hazard represented by SDHIs for aquatic organisms has long been recognized, as indicated in the specification sheets, and confirmed by recent data obtained for Danio rerio with boscalid or penthiopyrad [40, 41] and for Xenopus tropicalis embryos with isopyrazam or bixafen [42]. Simultaneously, the toxic effects of boscalid on honeybees have been demonstrated to occur as long as the duration of exposure is sufficient [43].…”

Section: Discussionmentioning

confidence: 61%

Evolutionarily conserved susceptibility of the mitochondrial respiratory chain to SDHI pesticides and its consequence on the impact of SDHIs on human cultured cells

et al. 2019

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Succinate dehydrogenase (SDH) inhibitors (SDHIs) are used worldwide to limit the proliferation of molds on plants and plant products. However, as SDH, also known as respiratory chain (RC) complex II, is a universal component of mitochondria from living organisms, highly conserved through evolution, the specificity of these inhibitors toward fungi warrants investigation. We first establish that the human, honeybee, earthworm and fungal SDHs are all sensitive to the eight SDHIs tested, albeit with varying IC50 values, generally in the micromolar range. In addition to SDH, we observed that five of the SDHIs, mostly from the latest generation, inhibit the activity of RC complex III. Finally, we show that the provision of glucose ad libitum in the cell culture medium, while simultaneously providing sufficient ATP and reducing power for antioxidant enzymes through glycolysis, allows the growth of RC-deficient cells, fully masking the deleterious effect of SDHIs. As a result, when glutamine is the major carbon source, the presence of SDHIs leads to time-dependent cell death. This process is significantly accelerated in fibroblasts derived from patients with neurological or neurodegenerative diseases due to RC impairment (encephalopathy originating from a partial SDH defect) and/or hypersensitivity to oxidative insults (Friedreich ataxia, familial Alzheimer’s disease).

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Section: Discussionmentioning

confidence: 61%

Evolutionarily conserved susceptibility of the mitochondrial respiratory chain to SDHI pesticides and its consequence on the impact of SDHIs on human cultured cells

et al. 2019

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“…Some pesticides may ameliorate lipid metabolism. For example, environmental doses of Boscalid, a widely used fungicide, induce gene expression that promotes β-oxidation and inhibits lipogenesis in the zebrafish liver [179]. Similarly, oral exposure to the carbamate fungicide propamocarb in mice during a 4-week period leads to a down regulation of genes involved in glycolysis, TG, and fatty acid synthesis in the liver [180].…”

Section: Oxidative Stress In Nafld: Role Of Pesticidesmentioning

confidence: 99%

“…Pesticide exposure may lead to NAFLD through an impact on lipid metabolism by (i) modifying FA uptake and efflux [171] and FFA transport, (ii) increasing lipogenesis [172][173][174] (Table 1), (iii) altering oxidation pathways [175] (Tables 1 and 2), and (iv) interacting with nuclear receptors involved in the control of metabolism [176][177][178]. Some pesticides may disrupt lipid metabolism [179,180].…”

mentioning

confidence: 99%

Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants

et al. 2020

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Non-alcoholic fatty liver disease (NAFLD) is often the hepatic expression of metabolic syndrome and its comorbidities that comprise, among others, obesity and insulin-resistance. NAFLD involves a large spectrum of clinical conditions. These range from steatosis, a benign liver disorder characterized by the accumulation of fat in hepatocytes, to non-alcoholic steatohepatitis (NASH), which is characterized by inflammation, hepatocyte damage, and liver fibrosis. NASH can further progress to cirrhosis and hepatocellular carcinoma. The etiology of NAFLD involves both genetic and environmental factors, including an unhealthy lifestyle. Of note, unhealthy eating is clearly associated with NAFLD development and progression to NASH. Both macronutrients (sugars, lipids, proteins) and micronutrients (vitamins, phytoingredients, antioxidants) affect NAFLD pathogenesis. Furthermore, some evidence indicates disruption of metabolic homeostasis by food contaminants, some of which are risk factor candidates in NAFLD. At the molecular level, several models have been proposed for the pathogenesis of NAFLD. Most importantly, oxidative stress and mitochondrial damage have been reported to be causative in NAFLD initiation and progression. The aim of this review is to provide an overview of the contribution of nutrients and food contaminants, especially pesticides, to oxidative stress and how they may influence NAFLD pathogenesis.

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“…The remaining issue to be resolved is to add Other recent reports revealed neurodevelopmental defects in zebrafish models after exposure of embryos to Bixafen or Boscalid a few hours post-fertilization [5,6] as well as severe cardiac toxicity [7]. Chronic exposures (28 days) of adult zebrafish led to alterations in carbohydrate and lipid metabolism, and induced damage in the kidneys and the liver [8]. A genotoxic effect was also shown in human cells after chronic exposure.…”

Section: Introductionmentioning

confidence: 99%

The Short-Term Exposure to SDHI Fungicides Boscalid and Bixafen Induces a Mitochondrial Dysfunction in Selective Human Cell Lines

et al. 2021

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Fungicides are used to suppress the growth of fungi for crop protection. The most widely used fungicides are succinate dehydrogenase inhibitors (SDHIs) that act by blocking succinate dehydrogenase, the complex II of the mitochondrial electron transport chain. As recent reports suggested that SDHI-fungicides could not be selective for their fungi targets, we tested the mitochondrial function of human cells (Peripheral Blood Mononuclear Cells or PBMCs, HepG2 liver cells, and BJ-fibroblasts) after exposure for a short time to Boscalid and Bixafen, the two most used SDHIs. Electron Paramagnetic Resonance (EPR) spectroscopy was used to assess the oxygen consumption rate (OCR) and the level of mitochondrial superoxide radical. The OCR was significantly decreased in the three cell lines after exposure to both SDHIs. The level of mitochondrial superoxide increased in HepG2 after Boscalid and Bixafen exposure. In BJ-fibroblasts, mitochondrial superoxide was increased after Bixafen exposure, but not after Boscalid. No significant increase in mitochondrial superoxide was observed in PBMCs. Flow cytometry revealed an increase in the number of early apoptotic cells in HepG2 exposed to both SDHIs, but not in PBMCs and BJ-fibroblasts, results consistent with the high level of mitochondrial superoxide found in HepG2 cells after exposure. In conclusion, short-term exposure to Boscalid and Bixafen induces a mitochondrial dysfunction in human cells.

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Toxic effects of boscalid in adult zebrafish (Danio rerio) on carbohydrate and lipid metabolism

Cited by 56 publications

References 55 publications

Evolutionarily conserved susceptibility of the mitochondrial respiratory chain to SDHI pesticides and its consequence on the impact of SDHIs on human cultured cells

Evolutionarily conserved susceptibility of the mitochondrial respiratory chain to SDHI pesticides and its consequence on the impact of SDHIs on human cultured cells

Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants

The Short-Term Exposure to SDHI Fungicides Boscalid and Bixafen Induces a Mitochondrial Dysfunction in Selective Human Cell Lines

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