Di (2-ethyl hexyl) phthalate (DEHP)-induced spleen toxicity in quail (Coturnix japonica) via disturbing Nrf2-mediated defense response

Yu, Lei; Li, Huixin; Guo, Jianying; Huang, Yue-Qiang; Wang, Hui; Talukder, Milton; Li, Jinlong

doi:10.1016/j.envpol.2019.05.061

Cited by 67 publications

(24 citation statements)

References 35 publications

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“…The formation and evolution of alcoholic fatty liver is inseparable from the ROS, inflammatory factors and oxidative stress induced by the liver during the metabolism of ethanol. The scientist knocked out the SIRT1 gene in the liver of mice fed with ethanol, activated downstream signal molecule Lipin-1 activity [10], and then up-regulated SREBP-1c and NFATc-4 proteins, eventually liver steatosis, inflammation and oxidative stress were evidently exacerbated [42]. Recent findings postulate that SIRT1 might be a specific target for ethanol to act in liver, and SIRT1-Lipin-1 mediated signaling plays a key role in the development of AFL [43,44].…”

Section: Discussionmentioning

confidence: 99%

Di (2-ethylhexyl) phthalate facilitates the progression of alcoholic fatty liver via mediating oxidative stress injury and lipid peroxidation in rats

Xu¹,

Ji²,

Zhao³

et al. 2020

Preprint

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Background: Long-term excessive drinking can cause various harms to the human body. Alcoholic fatty liver is the manifestation of early liver lesions mainly induced by alcohol. Di-(2-ethylhexyl) phthalate, as one of the environmental internal-secretion interfering-substance, is widely used in industrial processing and various consumer goods. Large quantities of epidemiological investigations and studies have shown that frequent exposure to high concentrations of DEHP may be a potential risk factor for liver function. Methods: We used DEHP to expose alcohol-induced fatty liver rats to study the effect of DEHP on alcoholic fatty liver. Results: The results found that DEHP exposure prominently accelerated hepatic steatosis, inflammation and oxidant stress, and activates signaling pathways involved in liver inflammation and oxidative stress-related proteins expression. Studies have suggested that cytochrome P450 2E1 and silent information regulator-1 are closely related to the occurrence of alcoholic fatty liver disease. Interestingly, the trend observed in the LO-2 cells assay was consistent with the in vivo conditions. Conclusions: DEHP may promote or aggravate the progression of alcoholic fatty liver disease through CYP2E1, SIRT1 and p38 mitogen-activated protein kinase (p38MAPK) / nuclear factor-kappa B signaling pathways. And this experimental study warns us that the environmental pollutants DEHP and its potential toxicity hazards to the human body are worthy of attention.

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Section: Discussionmentioning

confidence: 99%

Di (2-ethylhexyl) phthalate facilitates the progression of alcoholic fatty liver via mediating oxidative stress injury and lipid peroxidation in rats

Xu¹,

Ji²,

Zhao³

et al. 2020

Preprint

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“…Dietary antioxidants are vital for maintaining human health. There is accumulating evidence DEHP toxicity is associated with oxidative stress and depletion of antioxidants in several tissue including the spleen [5]. Supplementation with antioxidants therefore could retard oxidative injury and adverse effects of DEHP exposure.…”

Section: Discussionmentioning

confidence: 99%

“…The organ is susceptible to attack by environmental toxicants including DEHP. In a recent study, DEHP damaged the spleen of quail by dysregulating redox balance [5]. In the present study therefore, the role of Vit E in alleviating DEHP-induced alteration in hematological profile and toxicity in the spleen of Sprague Dawley rats was investigated.…”

Section: Introductionmentioning

confidence: 91%

“…DEHP founds application in floor tiles, wallpaper, raincoats, toys and auto upholstery [4]. Substantial amount of DEHP is used in the production of fragrance, cosmetics and condenser [5,6]. Moreover in Taiwan, DEHP is illegally used as a clouding agent in some processed foods including jams, jellies, fruit-flavored juices and beverages as well as in nutraceutical pills and powders [7,8].…”

Section: Introductionmentioning

confidence: 99%

“…In addition, studies in animals have shown that DEHP is carcinogenic [29]. Furthermore, it exerts potent toxic effects on the different organ in animals including kidney, testes, liver and spleen [5,30].…”

Section: Introductionmentioning

confidence: 99%

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Vitamin E Alleviates Diethylhexyl Phthalate-Induced Haemato-logical Changes and Splenic Oxidative Injury in Male Sprague-Dawley Rats

Akinwumi

2019

J. Can. Res. Updates

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Di-2-ethylhexyl phthalate (DEHP) is a ubiquitous environmental toxicant with high exposure potential to man mainly through leaching from water and foods plastics packages. Exposure to DEHP is associated with cancers, cardiovascular diseases, and splenic toxicity. In the present study, the effect of alpha tocopherol (α-tocopherol) on the DEHP-induced alteration in hematology and oxidative injury in the spleen of male Sprague Dawley rats was investigated. Animals were exposed daily for six weeks to 5 mg/kg bd.wt DEHP and 10 mg/kg bd.wt Vitamin E either alone or in combination. Control rats were given olive oil throughout the duration of the experiment. Organ weight indices and hematology parameters including packed cell volume (PCV), white blood cells (WBC), lymphocytes and neutrophils were determined in test and control rats. In addition, malondialdehyde, superoxide dismustase (SOD), catalase and glutathione-S-transferase (GST) activities were determined in the spleen. Histology of the spleen was also evaluated. Hematoxicity of DHEP was characterized by decreased PCV, WBC counts and neutrophil, while eosinophil was markedly elevated. DHEP administration resulted in oxidative stress that was manifested by elevated MDA and GST coupled with decreases in SOD and catalase activities. The spleen sections from DEHP-treated rats showed congestion and hyperplasia. However, Vitamin E modulated the hematological parameters and alleviated oxidative changes caused by DEHP exposure. Vitamin E also prevented DHEP associated lesions in the spleen. Therefore, Vitamin E could be useful in controlling hematotoxicty and splenic oxidative injury caused by DEHP intoxication.

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Curcumin alleviates bisphenol AF‐induced oxidative stress and apoptosis in caprine endometrial epithelial cells via the Nrf2 signaling pathway

Liu

Wang

et al. 2023

Environmental Toxicology

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Bisphenol AF (BPAF), a BPA‐substitute, has been widely used in industrial compounds throughout the world. Several studies have shown that BPAF has endocrine interference and reproductive toxicity. However, the toxic effects of BPAF on pregnancy and placenta of goats are still unclear. Therefore, the objective of this study was to reveal the toxic effect of BPAF by using an in vitro culture model of caprine endometrial epithelial cells (EECs) and further attempted to alleviate the toxicity by curcumin pretreatment. The results showed that BPAF induces significant effects on EECs, including decreased cell viability and mitochondrial membrane potential (△ψm), elevating intracellular reactive oxygen species (ROS), promoting cell apoptosis through upregulating the expression of Bax, Cytochrome c, and downregulating the expression of Bcl‐2. Meanwhile, BPAF induced dysregulation of oxidative stress by increasing the levels of malondialdehyde (MDA) and glutathione peroxidase (GSH‐Px) but decreasing the activities of superoxide dismutase (SOD). However, curcumin pretreatment could significantly attenuate BPAF‐induced toxic effects in EECs. Further study revealed that BPAF treatment could activate mitogen‐activated protein kinase (MAPK) pathway and nuclear factor‐erythroid 2‐related factor 2 (Nrf2) expression, but curcumin pretreatment significantly inhibited the activation of MAPK signal pathway and Nrf2 expression induced by BPAF. Overall, this study indicated that curcumin could prevent BPAF‐induced EECs cytotoxicity, which provides a potential therapeutic strategy for female infertility associated with BPAF exposure.

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Di (2-ethyl hexyl) phthalate (DEHP)-induced spleen toxicity in quail (Coturnix japonica) via disturbing Nrf2-mediated defense response

Cited by 67 publications

References 35 publications

Di (2-ethylhexyl) phthalate facilitates the progression of alcoholic fatty liver via mediating oxidative stress injury and lipid peroxidation in rats

Di (2-ethylhexyl) phthalate facilitates the progression of alcoholic fatty liver via mediating oxidative stress injury and lipid peroxidation in rats

Vitamin E Alleviates Diethylhexyl Phthalate-Induced Haemato-logical Changes and Splenic Oxidative Injury in Male Sprague-Dawley Rats

Curcumin alleviates bisphenol AF‐induced oxidative stress and apoptosis in caprine endometrial epithelial cells via the Nrf2 signaling pathway

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