Perinatal exposure to a dietary pesticide cocktail does not increase susceptibility to high-fat diet-induced metabolic perturbations at adulthood but modifies urinary and fecal metabolic fingerprints in C57Bl6/J mice

Smith, Lorraine; Klément, Wendy; Dopavogui, Léonie; Bock, Frédéric de; Lasserre, Frédèric; Barretto, Sharon Ann; Lukowicz, Céline; Fougerat, Anne; Polizzi, Arnaud; Schaal, Benoı̂st; Patris, Bruno; Denis, Colette; Feuillet, Guylène; Canlet, Cécile; Jamin, Emilien L.; Debrauwer, Laurent; Mselli-Lakhal, Laïla; Loiseau, Nicolas; Guillou, Hervé; Marchi, Nicola; Ellero‐Simatos, Sandrine; Gamet-Payrastre, Laurence

doi:10.1016/j.envint.2020.106010

Cited by 16 publications

(25 citation statements)

References 72 publications

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“…Lukowicz et al aimed to assess the toxicity of a mixture of six pesticides (boscalid, captan, chlorpyrifos, thiophanate, thiacloprid, and ziram) in mice, suggesting that pesticide treatment could affect the regular gut microbiota composition and the host metabolic homeostasis [ 110 ]. The perinatal exposure to a low-dose pesticide cocktail made up of six pesticides (chlorpyrifos, thiacloprid, thiophanate, captan, ziram and boscalid) administered to mice resulted in alterations in the urinary and faecal metabolite due to the alterations in the gut microbial communities [ 111 ].…”

Section: Pesticide Mixturesmentioning

confidence: 99%

Toxicology and Microbiota: How Do Pesticides Influence Gut Microbiota? A Review

Giambò

Teodoro

Costa

et al. 2021

IJERPH

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In recent years, new targets have been included between the health outcomes induced by pesticide exposure. The gastrointestinal tract is a key physical and biological barrier and it represents a primary site of exposure to toxic agents. Recently, the intestinal microbiota has emerged as a notable factor regulating pesticides’ toxicity. However, the specific mechanisms related to this interaction are not well known. In this review, we discuss the influence of pesticide exposure on the gut microbiota, discussing the factors influencing gut microbial diversity, and we summarize the updated literature. In conclusion, more studies are needed to clarify the host–microbial relationship concerning pesticide exposure and to define new prevention interventions, such as the identification of biomarkers of mucosal barrier function.

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Section: Pesticide Mixturesmentioning

confidence: 99%

Toxicology and Microbiota: How Do Pesticides Influence Gut Microbiota? A Review

Giambò

Teodoro

Costa

et al. 2021

IJERPH

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“…During this phase, food (mg/day) and water (ml/day) intake were closely monitored, and no significant differences were observed among the two groups (Table 1). This protocol was previously used by our research consortium (Smith et al, 2020). At weaning, all offspring were fed using standard control pellet and animals were kept in cages of 4 individuals.…”

Section: Mouse Perinatal Exposure Protocol and Pesticides Chow Preparationmentioning

confidence: 99%

“…At weaning, all offspring were fed using standard control pellet and animals were kept in cages of 4 individuals. The generation of the chow pellet containing pesticides is identical to the one we have previously described and used in (Klement et al, 2020;Lukowicz et al, 2018;Smith et al, 2020). The selected cocktail contains fungicides and insecticides (ziram, thiophanate, captan, chlorpyrifos, boscalid, and thiacloprid) that are relevant to agriculture, as suggested by the European Food Safety Authority reports (EFSA, 2018;Klement et al, 2020;Lukowicz et al, 2018;Smith et al, 2020).…”

Section: Mouse Perinatal Exposure Protocol and Pesticides Chow Preparationmentioning

confidence: 99%

“…Here, by using two distinct mouse and zebrafish models we provide evidence for an impact of maternal or developmental exposure to dietary and environmental pesticides on neuronal functions. In one model, C57BL6/j mice were fed immediately prior to and during mating, during pregnancy and lactation with chow pellets containing a cocktail of six pesticides, with relevance to agriculture (EFSA, 2018; Klement et al, 2020;Lukowicz et al, 2018;Smith et al, 2020) and exposing mice to the TDI for each pesticide. Using male and female offspring, we tracked behavior and in vivo brain electrophysiological outcomes.…”

Section: Introductionmentioning

confidence: 99%

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Varying modalities of perinatal exposure to a pesticide cocktail elicit neurological adaptations in mice and zebrafish

Forner-Piquer

Klément

Gangarossa

et al. 2021

Environmental Pollution

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Highlights 1) Perinatal pesticides links with long-term behavioral modifications in male mice.2) Behavioral changes are accompanied by electrographic brain slowing in vivo.3) In zebrafish larvae, pesticide cocktail elicited dose-dependent motor-behavioral changes.4) In zebrafish larvae, chlorpyriphos is a behavior-modifying pesticide contained in the cocktail.5) Non-lethal prenatal pesticide cocktail does not provoke brain malformations.

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“…However, the scientific literature does not cover the areas of multiple pesticide exposure and health consequences. In vivo studies on mixtures of pesticides have shown that dietary exposure may promote the occurrence of chronic diseases, but no mechanistic results are available to date [29,30]. The occurrence of CRC results from the interplay of genetic, environmental and microenvironmental factors [31].…”

Section: Introductionmentioning

confidence: 99%

Short-Term and Long-Term Carcinogenic Effects of Food Contaminants (4-Hydroxynonenal and Pesticides) on Colorectal Human Cells: Involvement of Genotoxic and Non-Genomic Mechanisms

Arnaud

Gauthier

Naour

et al. 2021

Cancers

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To investigate environmental impacts upon colorectal carcinogenesis (CRC) by diet, we assessed two western diet food contaminants: 4-hydroxynonenal (HNE), a major lipid peroxidation product neoformed during digestion, and a mixture of pesticides. We used human colonic cell lines ectopically eliciting varied genetic susceptibilities to CRC: the non-transformed human epithelial colonic cells (HCECs) and their five isogenic cell lines with the loss of APC (Adenomatous polyposis coli) and TP53 (Tumor protein 53) and/or ectopic expression of mutated KRAS (Kristen-ras). These cell lines have been exposed for either for a short time (2 -24 h) or for a long period (3 weeks) to 1 µM HNE and/or 10 µM pesticides. After acute exposure, we did not observe any cytotoxicity or major DNA damage. However, long-term exposure to pesticides alone and in mixture with HNE induced clonogenic transformation in normal HCECs, as well as in cells representing later stages of carcinogenesis. It was associated with genotoxic and non-genomic mechanisms (cell growth, metabolic reprogramming, cell mobility and epithelial-mesenchymal transition) depending on genetic susceptibility. This study demonstrated a potential initiating and promoting effect of food contaminants on CRC after long-term exposure. It supports that these contaminants can accelerate carcinogenesis when mutations in oncogenes or tumor suppressor genes occur.

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Perinatal exposure to a dietary pesticide cocktail does not increase susceptibility to high-fat diet-induced metabolic perturbations at adulthood but modifies urinary and fecal metabolic fingerprints in C57Bl6/J mice

Cited by 16 publications

References 72 publications

Toxicology and Microbiota: How Do Pesticides Influence Gut Microbiota? A Review

Toxicology and Microbiota: How Do Pesticides Influence Gut Microbiota? A Review

Varying modalities of perinatal exposure to a pesticide cocktail elicit neurological adaptations in mice and zebrafish

Short-Term and Long-Term Carcinogenic Effects of Food Contaminants (4-Hydroxynonenal and Pesticides) on Colorectal Human Cells: Involvement of Genotoxic and Non-Genomic Mechanisms

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