Effects of chronic glyphosate exposure to pregnant mice on hepatic lipid metabolism in offspring

Ren, Xin; Dai, Pengyuan; Perveen, Aneela; Tang, Qian; Zhao, Liangyu; Jia, Xiaofang; Li, Yansen; Li, Chunmei

doi:10.1016/j.envpol.2019.07.074

Cited by 31 publications

(7 citation statements)

References 39 publications

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“…Persistent but also non-persistent pesticides currently in use may also support the development of metabolic diseases [125,[131][132][133][134]. Experimental studies have allowed identification of the type of pesticides that promote fatty liver disease or changes in global metabolic homeostasis in animal models [123], such as organophosphorus or neonicotinoid or pyrethroid insecticides [135][136][137][138][139][140][141][142][143][144][145][146], triazine herbicides [147,148], glyphosate herbicides [149][150][151][152][153], or other families [154,155] and fungicides [152,[156][157][158][159][160][161] (Table 1).…”

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confidence: 99%

“…Experimental studies evaluating the consequences of pesticide exposure during the critical window of pre-and postnatal development (pregnancy and lactation) confirm that early life exposure to pesticides may have a role in metabolic disruption later in life (Table 1). A metabolic impact of perinatal exposure to pesticides in animal models has been reported for insecticides, such as chlorpyrifos [140,166] and imidacloprid [142]; herbicides, such as glyphosate [150] and 2-4 dichlorophenoxyacetic acid (2,4-D) [155]; and pesticide mixtures [167,168]. The metabolic consequences of early life exposure to organophosphate have been reviewed previously [61,74,169].…”

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confidence: 99%

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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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Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants

et al. 2020

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“…Secondly, an interesting result we obtained was a lower litter birth weight in Gly-exposed group in comparison to control at the expense of a decrease in male weight which deserve further study. Meanwhile, outbred mouse pups prenatally exposed to glyphosate or a GBH whose mother received a solution of 0.5% of the active ingredient in the drinking water during the 21 days of pregnancy showed a decreased body weight at weaning ( 174 ). Authors exposed that this effect could be explained by previous results obtained using the same experimental model where they detected a decrease in the body weight of mothers during pregnancy ( 36 ).…”

Section: Adverse Reproductive Outcomes Of Glyphosate and Its Formulationsmentioning

confidence: 99%

Glyphosate Herbicide: Reproductive Outcomes and Multigenerational Effects

et al. 2021

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Glyphosate base herbicides (GBHs) are the most widely applied pesticides in the world and are mainly used in association with GBH-tolerant crop varieties. Indiscriminate and negligent use of GBHs has promoted the emergence of glyphosate resistant weeds, and consequently the rise in the use of these herbicides. Glyphosate, the active ingredient of all GBHs, is combined with other chemicals known as co-formulants that enhance the herbicide action. Nowadays, the safety of glyphosate and its formulations remain to be a controversial issue, as evidence is not conclusive whether the adverse effects are caused by GBH or glyphosate, and little is known about the contribution of co-formulants to the toxicity of herbicides. Currently, alarmingly increased levels of glyphosate have been detected in different environmental matrixes and in foodstuff, becoming an issue of social concern. Some in vitro and in vivo studies have shown that glyphosate and its formulations exhibit estrogen-like properties, and growing evidence has indicated they may disrupt normal endocrine function, with adverse consequences for reproductive health. Moreover, multigenerational effects have been reported and epigenetic mechanisms have been proved to be involved in the alterations induced by the herbicide. In this review, we provide an overview of: i) the routes and levels of human exposure to GBHs, ii) the potential estrogenic effects of glyphosate and GBHs in cell culture and animal models, iii) their long-term effects on female fertility and mechanisms of action, and iv) the consequences on health of successive generations.

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“…Pathological changes in iron levels and oxidative stress was shown to be involved in the mechanisms of glyphosate hepatotoxicity (Tang et al 2017). It was also demonstrated that chronic prenatal exposure to glyphosate in mice can result in hepatic lipid metabolism disruption in the offspring (Ren et al 2019). Oxidative stress and iron overload are important biomarkers of hepatic function, being important targets for biomonitoring glyphosate exposure.…”

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confidence: 99%

Perinatal Exposure to a Glyphosate Pesticide Formulation Induces Liver Damage in Immature Rat Pups

Rieg¹,

Cattani²,

Naspolini³

et al. 2021

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The present study investigated the effects of perinatal exposure to glyphosate-based herbicide (GBH) on liver of immature Wistar rats. Female rats were exposed to GBH (70 mg glyphosate/Kg body weight/day) in drinking water from gestation day 5 and continually up to lactation day 15. The perinatal exposure to GBH increased 45Ca2+ influx in offspring’s liver Pharmacological tools indicated a role played by oxidative stress, phospholipase C (PLC) and Akt pathways, as well as voltage-dependent Ca2+ channel modulation to GBH-induced Ca2+ influx in liver. In addition, changes in the enzymatic antioxidant defense system, decreased GSH content, lipid peroxidation and protein carbonylation suggest a connection between GBH hepatotoxic mechanism and redox imbalance. The perinatal exposure to GBH also increased the enzymatic activities of transaminases and gamma-glutamyl transferase in offspring's liver and blood, suggesting a pesticide-induced liver injury. Moreover, we detected increased iron levels in liver, blood and bone marrow of GBH-exposed rats, which were accompanied by increased transferrin saturation and decreased transferrin levels in blood. The levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were increased in the liver of rats exposed to GBH. We also detected increased phospho-p65NFκB immunocontent, corresponding to the active form of this transcription factor. Therefore, we propose that excessive amounts of iron induced by perinatal exposure to GBH in offspring’s liver, blood and bone marrow may account for iron-driven hepatotoxicity, which was associated with Ca2+ influx, oxidative damage and inflammation in immature rats. Further studies will clarify whether these events can ultimately impact on liver function.

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Effects of chronic glyphosate exposure to pregnant mice on hepatic lipid metabolism in offspring

Cited by 31 publications

References 39 publications

Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants

Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants

Glyphosate Herbicide: Reproductive Outcomes and Multigenerational Effects

Perinatal Exposure to a Glyphosate Pesticide Formulation Induces Liver Damage in Immature Rat Pups

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