Bisphenol A Exposure Enhances Atherosclerosis in WHHL Rabbits

Fang, Chao; Niu, Bo; Waqar, Ahmed Bilal; Niimi, Manabu; Shen, Li; Satoh, Keisuke; Shiomi, Masashi; Ye, Ting; Dong, Shuang; Fan, Jianglin

doi:10.1371/journal.pone.0110977

Cited by 49 publications

(59 citation statements)

References 54 publications

(75 reference statements)

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“…Administration of BPA (40 mg·kg −1 ·day −1 , gavage, 8 weeks) to hyperlipidemic rabbits induced atherosclerosis, infiltration of inflammatory cells to the myocardium, myocardial infarction, and calcification (Fang et al, ). BPA exposure (0.4 mg·kg −1 ·day −1 , gavage, 12 weeks) in hyperlipidemic rabbits enhanced atherosclerosis in both aorta and left coronary arteries (Fang et al, ). In another study, BPA administration (50 mg/kg, in diet, for 12 weeks) to pregnane X receptor‐humanized ApoE deficient mice increased atherosclerosis in the aortic root and brachiocephalic artery (Sui et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…The other study reported that BPA exposure (2 mg·kg −1 ·day −1 , i.p., for 4 weeks) increased TC and LDL‐C concomitant with an increase in the body weight in male mice (Moghaddam, Samarghandian, & Farkhondeh, ). Fang and his colleagues () reported administration of BPA (0.4 mg·kg −1 ·day −1 , gavage, 12 weeks) to hyperlipidemic rabbits increased adiposity and induced adipocytes hypertrophy with no effects on the body weight (Fang et al, ). Previously, it has been reported that BPA by affecting on the expression of some genes evokes an important role in adipocytes differentiation, function, white adipose tissue weight, and obese phenotype in rodents.…”

Section: Discussionmentioning

confidence: 99%

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Vitis vinifera (grape) seed extract and resveratrol alleviate bisphenol‐A‐induced metabolic syndrome: Biochemical and molecular evidences

Rameshrad

Razavi

Imenshahidi

et al. 2019

Phytotherapy Research

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The mechanisms of bisphenol‐A (BPA)‐induced metabolic syndrome as well as the protective role of grape seed extract (GSE) and resveratrol were investigated. Rats were treated with BPA (0 and 35 mg·kg−1·day−1, gavage) plus resveratrol (25, 50, and 100 mg·kg−1·day−1, i.p.) or GSE (3, 6, 12 mg·kg−1·day−1, i.p.) or vitamin E (200 IU/kg/every other day, i.p.). After 2 months, mean systolic blood pressure, serum lipid profile, glycaemia, and fat index were examined. By enzyme‐linked immunosorbent assay, the serum concentrations of insulin, leptin, adiponectin, and paraoxonase 1, and by real‐time polymerase chain reaction as well as western blotting, key liver elements in cholesterol hemostasis (LDLR, CYP7A1, ABCG5 and 8) and insulin signaling (p‐Akt/Akt and p‐PI3K/PI3K) were measured. BPA increased mean systolic blood pressure, total cholesterol, and low‐density lipoprotein cholesterol and reduced paraoxonase1 and the hepatic expression of both ABCG5 and ABCG8. It increased the body fat index, leptin, adiponectin, insulin, and glycaemia level and decreased the hepatic protein expression of p‐Akt/Akt and p‐PI3K/PI3k. GSE, resveratrol, or vitamin E coadministration along with BPA restored the detrimental effects of BPA in some levels. Herein, the predisposing effects of BPA‐induced metabolic syndrome were restored by GSE and resveratrol, linked to the regulation of insulin signaling, ABCG8 expression, and their antioxidant properties.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Vitis vinifera (grape) seed extract and resveratrol alleviate bisphenol‐A‐induced metabolic syndrome: Biochemical and molecular evidences

Rameshrad

Razavi

Imenshahidi

et al. 2019

Phytotherapy Research

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“…The adverse effects of BPA have been largely related to its estrogenic activity, which results in disturbed reproductive function, steroidogenesis, and adipogenesis. However, BPA has non‐estrogenic effects, such as the promotion of atherosclerosis in rabbits and endoplasmic reticulum stress in cultured endothelial cells …”

Section: Introductionmentioning

confidence: 99%

“…However, BPA has non-estrogenic effects, such as the promotion of atherosclerosis in rabbits and endoplasmic reticulum stress in cultured endothelial cells. 13 Two key consequences of CKD are the higher risks of CKD progression and of cardiovascular disease. In fact, this higher risk was used to set the thresholds of glomerular filtration rate and albuminuria that define CKD.…”

mentioning

confidence: 99%

Bisphenol A is an exogenous toxin that promotes mitochondrial injury and death in tubular cells

Bosch-Panadero¹,

Mas²,

Civantos

et al. 2017

Environmental Toxicology

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“…Likewise, cumulative data suggested a link between BPA and cardiovascular disorders and chronic diseases [34,35], but the causal relationship and the underlying mechanisms are unclear. Studies using various strains of transgenic mice and rabbits revealed that BPA aggravates atherosclerosis [36][37][38][39][40]. Numerous studies in rodents evidenced that BPA exposure induces the generation of reactive oxygen species and causes hepatotoxicity [41][42][43][44].…”

mentioning

confidence: 99%

The Mechanism of Bisphenol A Atherogenicity Involves Apolipoprotein A-I Downregulation through NF-κB Activation

Trusca¹,

Dumitrescu²,

Fenyo³

et al. 2019

IJMS

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Apolipoprotein A-I (apoA-I) is the major protein component of high-density lipoproteins (HDL), mediating many of its atheroprotective properties. Increasing data reveal the pro-atherogenic effects of bisphenol A (BPA), one of the most prevalent environmental chemicals. In this study, we investigated the mechanisms by which BPA exerts pro-atherogenic effects. For this, LDLR −/− mice were fed with a high-fat diet and treated with 50 µg BPA/kg body weight by gavage. After two months of treatment, the area of atherosclerotic lesions in the aorta, triglycerides and total cholesterol levels were significantly increased, while HDL-cholesterol was decreased in BPA-treated LDLR −/− mice as compared to control mice. Real-Time PCR data showed that BPA treatment decreased hepatic apoA-I expression. BPA downregulated the activity of the apoA-I promoter in a dose-dependent manner. This inhibitory effect was mediated by MEKK1/NF-κB signaling pathways. Transfection experiments using apoA-I promoter deletion mutants, chromatin immunoprecipitation, and protein-DNA interaction assays demonstrated that treatment of hepatocytes with BPA induced NF-κB signaling and thus the recruitment of p65/50 proteins to the multiple NF-κB binding sites located in the apoA-I promoter. In conclusion, BPA exerts pro-atherogenic effects downregulating apoA-I by MEKK1 signaling and NF-κB activation in hepatocytes. Int. J. Mol. Sci. 2019, 20, 6281 2 of 15 and in apoA-I −/− /LDLR −/− mice [6]. On the other hand, overexpression of human apoA-I reduced atherogenesis in apoE −/− or in LDLR −/− mice [7][8][9][10][11][12][13][14], providing strong evidence for the antiatherogenic role of apoA-I. Recently, it was proposed that the ratio of HDL-cholesterol to apoA-I gives additional insights as a risk marker for cardiovascular disease [15]. To exploit the anti-atherogenic properties of HDL-apoA-I, different approaches, such as pharmacological interventions using HDL-apoA-I mimetic peptides or infusions of apoA-I-containing particles were proposed for the reduction of atherogenesis [16,17].In humans, the APOAI gene is 1.8 Kb in length and it is located on chromosome 11 in the APOAI/APOCIII/APOAIV gene cluster [18]. ApoA-I is synthesized mainly by the liver and the small intestine. APOAI gene expression is mainly regulated at transcriptional level [19]. The APOAI gene promoter contains a TATA box and several cis elements that regulate its gene expression in either a positive or negative manner. Acidosis caused apoA-I downregulation by promoting binding of repressor proteins to a pH-responsive element that overlaps the TATA box within the apoA-I promoter [20]. Several hormones, such as glucocorticoids, thyroid hormones, and insulin, induced APOAI gene expression through a direct mechanism interacting with their specific hormone response elements [21,22]. In humans, treatment with fibrates that interact with a PPAR-responsive element located in the apoA-I promoter increased APOAI gene expression, but opposite effects of fibrates on apoA-I expression were found in r...

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Bisphenol A Exposure Enhances Atherosclerosis in WHHL Rabbits

Cited by 49 publications

References 54 publications

Vitis vinifera (grape) seed extract and resveratrol alleviate bisphenol‐A‐induced metabolic syndrome: Biochemical and molecular evidences

Vitis vinifera (grape) seed extract and resveratrol alleviate bisphenol‐A‐induced metabolic syndrome: Biochemical and molecular evidences

Bisphenol A is an exogenous toxin that promotes mitochondrial injury and death in tubular cells

The Mechanism of Bisphenol A Atherogenicity Involves Apolipoprotein A-I Downregulation through NF-κB Activation

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