Bottom-line mechanism of organochlorine pesticides on mitochondria dysfunction linked with type 2 diabetes

Ko, Eun Jung; Choi, Moonsung; Shin, Sooim

doi:10.1016/j.jhazmat.2020.122400

Cited by 27 publications

(7 citation statements)

References 36 publications

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“…Dysfunctions of this basic process have been linked to a variety of disorders and the onset of old age (Niccoli et al, 2012). Even if pesticides were only intended to harm plants, fungi, or insects, there is now growing evidence that they can impair mammals' mitochondria and create abnormalities in energy metabolism, which can lead to disease and neurotoxicity (Farkhondeh et al, 2020;Ko et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Deterioration of Cytochrome C Content and Mitochondrial Dysfunction in Brain of Male Rats after Sub-Chronic Exposure to Thiamethoxam and Protective Role of N- Acetylcysteine

Abdel-Razik

Mosallam

Hamed

2022

Alexandria Science Exchange Journal

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Mitochondria sustain healthy brain function. Herein we aimed to evaluate the thiamethoxam (MX) effect on the rat brain mitochondria in addition to the protective role of N-acetylcysteine (NAC) against MX harmful effects. Thiamethoxam was administered orally with five doses each week for 28 days to male albino rats at 1/50 of the LD50 (31.26 mg/kg bw). The results demonstrated that the thiamethoxam neurotoxicity was confirmed by the significant rising in acetylcholinesterase, and lactate dehydrogenase activities of plasma. A significant increase in mitochondrial antioxidants as superoxide dismutase and reduced glutathione was found. Also, significant induction of the oxidative stress and DNA damage via rising the malondialdehyde, and 8-hydroxy-2'-deoxyguanosine biomarkers was recorded by 32.5% and 118.61% respectively. Substantial depression in mitochondrial NADH dehydrogenase, cytochrome c reductase, cytochrome c oxidase, and Mg 2+ ATPase complexes as well as 23 % cerebral infarction was manifested by histological evaluation using the dehydrogenase activity indicator, 2, 3, 5-triphenyl tetrazolium chloride staining. In conclusion, MX can pose a hazard to the integrity and functioning of rats' brain mitochondria, perhaps leading to neurodegenerative disorders. Additionally, earlier treatment of the synthetic antioxidant N-acetylcysteine could prove beneficial in combating the harmful effects of thiamethoxam.

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Section: Introductionmentioning

confidence: 99%

Deterioration of Cytochrome C Content and Mitochondrial Dysfunction in Brain of Male Rats after Sub-Chronic Exposure to Thiamethoxam and Protective Role of N- Acetylcysteine

Abdel-Razik

Mosallam

Hamed

2022

Alexandria Science Exchange Journal

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“…However, complex III activities in males were unchanged in all groups. In our previous study, we found that OCPs exert a competitive inhibitory action on complex III in isolated hepatic mitochondria [37]. According to these results, OCPs and the mixtures of OCPs with Aroclor are expected to have an effect similar to that of a specific inhibitor of complex III in the tail (muscular) mitochondria of females.…”

Section: Inhibition Of Mitochondrial Complex III Activity Upon Exposure To Pops In Femalesmentioning

confidence: 86%

Mixed Exposure of Persistent Organic Pollutants Alters Oxidative Stress Markers and Mitochondrial Function in the Tail of Zebrafish Depending on Sex

Lee

et al. 2021

IJERPH

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Persistent organic pollutants (POPs) are lipid-soluble toxins that are not easily degraded; therefore, they accumulate in the environment and the human body. Several studies have indicated a correlation between POPs and metabolic diseases; however, their effects on mitochondria as a central organelle in cellular metabolism and the usage of mitochondria as functional markers for metabolic disease are barely understood. In this study, a zebrafish model system was exposed to two subclasses of POPs, organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs), under two different conditions (solitary OCPs or OCPs with PCBs (Aroclor 1254)), and changes in the oxidative stress marker levels and mitochondrial enzyme activities in the electron transport chain of the tail were measured to observe the correlation between POPs and representative biomarkers for metabolic disease. The results indicated different responses upon exposure to OCPs and OCPs with Aroclor 1254, and accelerated toxicity was observed following exposure to mixed POPs (OCPs with Aroclor 1254). Males were more sensitive to changes in the levels of oxidative stress markers induced by POP exposure, whereas females were more susceptible to the toxic effects of POPs on the levels of mitochondrial activity markers. These results demonstrate that the study reflects real environmental conditions, with low-dose and multiple-toxin exposure for a long period, and that POPs alter major mitochondrial enzymes’ functions with an imbalance of redox homeostasis in a sex-dependent manner.

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“…These results suggest that OCPs may disrupt lipid metabolism and contribute to dyslipidemia, which is in line with previous studies. Exposure to persistent organic pollutants, especially OCPs, may alter genome-wide gene transcription related to energy metabolism [7,17] and induce mitochondrial dysfunction [35,36], thus affecting the metabolites of crucial metabolic processes mainly related to human lipid metabolism [37]. Lee et al observed signi cant associations of serum p,p′-DDE with higher TGs and lower HDL during a 20-year follow-up study [38].…”

Section: Discussionmentioning

confidence: 99%

Associations of Dietary Exposure to Organochlorine Pesticides from Plant-origin Foods with Lipid Metabolism and Inflammation in Childbearing-age Women: A Multiple Follow-up Study in North China

Wang

Gao

Tan

et al. 2021

Preprint

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Background Potential links between population exposure to organochlorine pesticides (OCPs) and their impact on human health are under discussion. The current study explored the effects of population OCP intake from plant-origin food consumption on lipid metabolism and inflammation using a multiple follow-up study. Methods A total of 10 childbearing-age women (five in urban areas and five in rural areas) in northern China were recruited and visited for five times. During each visit, we conducted a questionnaire survey, blood collection, and food sampling. The levels of OCPs in cereals, fruits, and vegetables were measured, and nutrient content information was obtained from a national monitoring program. We calculated the women’s dietary intakes of OCPs and nutrients. Serum biomarkers of lipids [triglycerides, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL), and lipoprotein(a)], monocyte chemotactic protein-1, interleukin (IL)-6, and IL-8 were measured. Linear mixed-effect models were used to evaluate the associations of dietary OCP and nutrient intake with serum biomarkers. Results The dietary intake of p,p′-dichlorodiphenyltrichloroethane (DDT) [β = -10.11, 95% confidence interval (95%CI): -17.32, -2.905] and o,p′-dichlorodiphenyldichloroethylene (DDE) (β = -6.077, 95%CI: -9.954, -2.200) were overall negatively associated with serum HDL, whereas other OCPs were not. IL-8 was positively associated with intake of dieldrin (β = 0.390, 95% CI: 0.105, 0.674), endosulfan-β (β = 0.361, 95%CI: 0.198, 0.523), total endosulfan (β = 0.136, 95%CI: 0.037, 0.234), and total OCPs (β = 0.084, 95%CI: 0.016, 0.153), and negatively correlated with intake of p,p′-DDE (β = -2.692, 95%CI: -5.185, -0.198). No associations between dietary nutrient intake and serum biomarkers were observed. Conclusions We concluded that dietary intake of some individual DDT-, DDE- dieldrin-, and endosulfan-class chemicals from plant-origin foods may interfere with lipid metabolism and inflammation responses.

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Bottom-line mechanism of organochlorine pesticides on mitochondria dysfunction linked with type 2 diabetes

Cited by 27 publications

References 36 publications

Deterioration of Cytochrome C Content and Mitochondrial Dysfunction in Brain of Male Rats after Sub-Chronic Exposure to Thiamethoxam and Protective Role of N- Acetylcysteine

Deterioration of Cytochrome C Content and Mitochondrial Dysfunction in Brain of Male Rats after Sub-Chronic Exposure to Thiamethoxam and Protective Role of N- Acetylcysteine

Mixed Exposure of Persistent Organic Pollutants Alters Oxidative Stress Markers and Mitochondrial Function in the Tail of Zebrafish Depending on Sex

Associations of Dietary Exposure to Organochlorine Pesticides from Plant-origin Foods with Lipid Metabolism and Inflammation in Childbearing-age Women: A Multiple Follow-up Study in North China

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