Serum bisphenol A and progression of type 2 diabetic nephropathy: a 6-year prospective study

Hu, Jinbo; Wang, Yue; Goswami, Richa; Peng, Chuan; Gao, Rufei; Huang, Zhou; Zhang, Yi; Cheng, Qingfeng; Zhen, Qianna; Li, Qifu

doi:10.1007/s00592-015-0801-5

Cited by 36 publications

(28 citation statements)

References 24 publications

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“…Apart from this, it should be noted that uric acid clearance does not decrease in proportion to the glomerular filtration rate in chronic kidney disease (40). Even though exposure of BPA decreases the glomerular filtration rate, the compensatory increase in uric acid excretion per nephron may help to maintain a normal level of uric acid clearance (11, 23, 39, 40).…”

Section: Discussionmentioning

confidence: 99%

“…Hyperuricemia was defined as a serum uric acid concentration greater than 420 mM in men and 360 mΜ in women. Serum concentrations of BPA were measured with a commercially available ELISA kit (IBL, Gunma, Japan) designed for the quantitative determination of BPA in human serum samples (11,23). The measurement range is 0.3-100 ng/ml.…”

Section: Matched Case-control Studymentioning

confidence: 99%

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Bisphenol A promotes hyperuricemia via activating xanthine oxidase

et al. 2018

FASEB j.

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The prevalence of hyperuricemia has increased rapidly over the past decades. Bisphenol A (BPA) is an environmental endocrine disruptor. We investigated the effects of BPA on uric acid metabolism and its potential mechanisms. Experiments were performed in different animal models, cell cultures, and humans. In 3 different animal models, BPA exposure increased serum and hepatic uric acid with enhanced activity of xanthine oxidase (XO) in liver, whereas the excretion of uric acid was unchanged. Both in vivo and in vitro, BPA-induced uric acid production was decreased after treatment with allopurinol, which is a XO inhibitor. XO led to the accumulation of uric acid after xanthine was added, with the enzyme-catalyzed reaction, which was enhanced by BPA. Altered secondary structures of XO were found by circular dichroism analysis in the conditions of different BPA concentrations. Molecular docking portrayed Asp360 and Lys422 of XO to be the preferred binding sites for BPA. Mutation of both sites significantly blocked the effect of BPA on XO activity. In humans, patients with hyperuricemia exhibited higher levels of serum BPA than subjects without hyperuricemia. These findings demonstrate BPA promotes hyperuricemia by increasing hepatic uric acid synthesis via the activation of XO, probably through direct binding.-Ma, L., Hu, J., Li, J., Yang, Y., Zhang, L., Zou, L., Gao, R., Peng, C., Wang, Y., Luo, T., Xiang, X., Qing, H., Xiao, X., Wu, C., Wang, Z., He, J. C., Li, Q., Yang, S. Bisphenol A promotes hyperuricemia via activating xanthine oxidase.

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Section: Discussionmentioning

confidence: 99%

Section: Matched Case-control Studymentioning

confidence: 99%

Bisphenol A promotes hyperuricemia via activating xanthine oxidase

et al. 2018

FASEB j.

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“…Since we did not find reduction of cell viability with 10 −9 mol/L BPA, suggesting that BPA is not toxic for PCCL3 cells at this concentration, we decided to perform the next experiments using this concentration. Moreover, literature data suggest that the concentration of BPA in the serum is in nmol/L range in humans ( 33 , 34 ). Results were expressed as relative to control.…”

Section: Methodsmentioning

confidence: 99%

Bisphenol A increases hydrogen peroxide generation by thyrocytes both in vivo and in vitro

Silva

Xavier

Gonçalves

et al. 2018

Endocrine Connections

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Bisphenol A (BPA) is the most common monomer in polycarbonate plastics and an endocrine disruptor. Though some effects of BPA on thyroid hormone (TH) synthesis and action have been described, the impact of this compound on thyroid H2O2 generation remains elusive. H2O2 is a reactive oxygen species (ROS), which could have deleterious effect on thyrocytes if in excess. Therefore, herein we aimed at evaluating the effect of BPA exposition both in vivo and in vitro on H2O2 generation in thyrocytes, besides other essential steps for TH synthesis. Female Wistar rats were treated with vehicle (control) or BPA 40 mg/kg BW for 15 days, by gavage. We then evaluated thyroid iodide uptake, mediated by sodium-iodide symporter (NIS), thyroperoxidase (TPO) and dual oxidase (DOUX) activities (H2O2 generation). Hydrogen peroxide generation was increased, while iodide uptake and TPO activity were reduced by BPA exposition. We have also incubated the rat thyroid cell line PCCL3 with 10−9 M BPA and evaluated Nis and Duox mRNA levels, besides H2O2 generation. Similar to that found in vivo, BPA treatment also led to increased H2O2 generation in PCCL3. Nis mRNA levels were reduced and Duox2 mRNA levels were increased in BPA-exposed cells. To evaluate the importance of oxidative stress on BPA-induced Nis reduction, PCCL3 was treated with BPA in association to N-acetylcysteine, an antioxidant, which reversed the effect of BPA on Nis. Our data suggest that BPA increases ROS production in thyrocytes, what could lead to oxidative damage thus possibly predisposing to thyroid disease.

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“…The EIMDS aimed at evaluating the influence of environmental and inflammatory factors on metabolic diseases such as obesity, type 2 diabetes, hypertension and chronic kidney disease [9,10]. Essential hypertension was defined as an average blood pressure ≥140/90 mmHg on at least two different occasions, without any evidence of secondary hypertension.…”

Section: Patientsmentioning

confidence: 99%

Association Between Serum Cortisol and Chronic Kidney Disease in Patients with Essential Hypertension

Xiang²,

Hu³

et al. 2016

Kidney Blood Press Res

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Background/Aims: Serum cortisol level is elevated in patients with essential hypertension. We aimed at investigating the association of serum cortisol levels with parameters of renal function in essential hypertension. Methods: One hundred and seventy-eight patients with essential hypertension participated in the study. Fasting serum samples were collected at 8:00 am. Renal function was measured as estimated glomerular filtration rate (eGFR) calculated by the Chronic Kidney Disease Epidemiology Collaboration creatinine- cystatin C equation (eGFRcr-cys). Correlation analysis and stepwise regression analysis were used to detect the relationship between cortisol and eGFRcr-cys. The distributions of serum cortisol were split by the tertiles and subjects were stratified into those with low, median and high levels accordingly. Results: Serum cortisol levels were significantly higher in subjects whose eGFRcr-cys<90 ml/min/1.73 m² than subjects whose eGFRcr-cys>90 ml/min/1.73 m² (394.0±93.4 vs. 343.2±98.4 nmol/L, P=0.001). Age, systolic blood pressure, and serum total cholesterol, uric acid, cortisol levels were significantly associated with eGFRcr-cys, serum levels of creatinine and cystatin C. After adjusting for clinical factors, serum cortisol level had a statistically significant negative association with the eGFRcr-cys (β=-0.19, P=0.027), and positive associations with cystatin C (β=0.31, P=0.001) and creatinine (β=0.14, P=0.044). With the increment of cortisol tertile, the eGFRcr-cys significantly decreased (93.18±14.36 vs. 84.61±14.67 vs. 81.29±12.36 ml/min/1.73 m² for low, median and high tertile, respecively, P=0.001). Conclusion: Serum cortisol level was negatively correlated with eGFRcr-cys in subjects with essential hypertension. Further studies are needed to investigate whether cortisol plays a role in hypertensive nephropathy development.

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Serum bisphenol A and progression of type 2 diabetic nephropathy: a 6-year prospective study

Abstract: Serum BPA may be a predictor of CKD in patients with T2D.

Cited by 36 publications

References 24 publications

Bisphenol A promotes hyperuricemia via activating xanthine oxidase

Bisphenol A promotes hyperuricemia via activating xanthine oxidase

Bisphenol A increases hydrogen peroxide generation by thyrocytes both in vivo and in vitro

Association Between Serum Cortisol and Chronic Kidney Disease in Patients with Essential Hypertension

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