Insecticide Exposure and Development of Nonalcoholic Fatty Liver Disease

Yang, Jason Szuhao; Park, Yeonhwa

doi:10.1021/acs.jafc.8b03177

Cited by 20 publications

(16 citation statements)

References 40 publications

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“…This pesticide is commonly used in agricultural and household [4,5]. In 2012, there was at least over 1 billion pound of pesticides usage in worldwide and it has dramatically increased for the last two decades [6,7]. Due to the widespread use of this chemical substance in agricultural and household, its residues in food may be harmful to non-targeting organisms, especially humans [8,9].…”

Section: Introductionmentioning

confidence: 99%

“…Carbofuran contamination has caused many negative effects on organism such as an oxidative stress and impairment on motoric, cognitive, and memory functions [3,10]. Some studies have also proven that carbofuran effects are significantly harmful on the liver functions, especially result in the Non-Alcoholic Fatty Liver Disease (NAFLD) [7,11]. The dysfunction of the liver has become a serious illness in human considering that the liver is one of the important organs.…”

Section: Introductionmentioning

confidence: 99%

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The effects of laser diode treatment on liver dysfunction of Mus musculus due to carbofuran exposure: An in vivo study

Astuti¹,

Victory²,

Mahmud³

et al. 2019

J Adv Vet Anim Res

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Objective:The aim of this study is to determine the effect of laser diode as an alternative treatment on liver dysfunction (in vivo study) that is caused by carbofuran using male mice (Mus musculus) strain Balb/C.Materials and Methods:The samples were divided into three groups, namely, Group C–L– (control group, no treatment), Group C+L– (only treated by carbofuran treatment), and Group C+L+ (treatment group, treated by carbofuran and laser-puncture) with five replications each. After being treated, each liver slice of samples was observed using microscope to get the histology result and then scored.Results:Carbofuran contamination can lead to inflammation of cells and necrosis. The histology results and the scoring test showed that the liver cells repair with the energy dose of laser diode at 0.5 and 1.0 Joule.Conclusion:The optimum energy dose in this study was 1.0 Joule which had the closest score of inflammatory cells and necrosis to normal liver cells.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effects of laser diode treatment on liver dysfunction of Mus musculus due to carbofuran exposure: An in vivo study

Astuti¹,

Victory²,

Mahmud³

et al. 2019

J Adv Vet Anim Res

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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).…”

mentioning

confidence: 99%

“…Pesticides alter glucose metabolism through the activation of glucose uptake, glycogenolysis, gluconeogenesis (for insecticides, see [136]; for diazinon or monocrotophos-treated animals, see [181][182][183], or inhibition of the mitochondrial respiratory chain [184]. They also have exerted effects through modulation of carbohydrate response element binding protein (Chrebp) gene expression levels [185] and changes in the expression of peroxisome proliferator-activated receptor (PPAR)β/δ and genes involved in glucose metabolism (FoxO1 and cAMP response element-binding protein, Creb) [186].…”

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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“…Despite increasing concerns about pesticide residues in food products and water, various pesticides have been widely used to control plant diseases and improve crop yield. A previous study showed that insecticide exposure impaired lipid metabolism, thereby resulting in the development of NAFLD [21]. Moreover, recent studies have reported that fungicides such as propiconazole, flutriafol, cyproconazole, dazomet, fluazinam, hexaconazole, pyrasulfotole metabolite, and myclobutanil can cause NAFLD pathogenesis [22][23][24][25].…”

Section: Discussionmentioning

confidence: 99%

Tebuconazole Fungicide Induces Lipid Accumulation and Oxidative Stress in HepG2 Cells

Kwon

Kim

Jeong³

et al. 2021

Foods

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Tebuconazole (TEB), a triazole fungicide, is frequently applied to agriculture for the increase of food production. Although TEB causes liver toxicity, its effects on cellular lipid accumulation are rarely investigated. Therefore, this study aimed to study the effects of TEB on lipid metabolism and accumulation in HepG2 cells. HepG2 cells were exposed to 0–320 µM TEB for 1–24 h. TEB (20–80 µM, 24 h)-treated cells showed lipid accumulation. Further, TEB (20–80 µM, 1–12 h) increased the nuclear translocation of peroxisome proliferator-activated receptors and the expression of lipid uptake and oxidation-related markers such as cluster of differentiation 36, fatty acid transport protein (FATP) 2, FATP5, and carnitine palmitoyltransferase 1. Oxidative stress levels in TEB-treated cells (20–80 µM, 24 h) were higher, compared to those in the control. TEB (20–80 µM, 24 h) also induced the loss of mitochondrial membrane potential and lower levels of microsomal triglyceride transfer protein in the cells. Thus, TEB can induce lipid accumulation by altering the expression of lipid-metabolizing molecules and can therefore impair lipid metabolism. Our data suggest that human exposure to TEB may be a risk factor for non-alcoholic fatty liver disease.

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Insecticide Exposure and Development of Nonalcoholic Fatty Liver Disease

Cited by 20 publications

References 40 publications

The effects of laser diode treatment on liver dysfunction of Mus musculus due to carbofuran exposure: An in vivo study

The effects of laser diode treatment on liver dysfunction of Mus musculus due to carbofuran exposure: An in vivo study

Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants

Tebuconazole Fungicide Induces Lipid Accumulation and Oxidative Stress in HepG2 Cells

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