Vitamin C coadministration augments bisphenol A, nonylphenol, and octylphenol induced oxidative damage on kidney of rats

Korkmaz, Ali; Aydoğan, Müfide; Kolankaya, Dürdane; Barlas, Nurhayat

doi:10.1002/tox.20556

Cited by 48 publications

(32 citation statements)

References 44 publications

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“…ALP is released in blood stream when liver is damaged or when there is biliary obstruction (Kako et al, ). Korkmaz et al () have also reported alteration in LFT markers as a result of exposure to EDCs such as BPA, nonylphenol, and octylphenol.…”

Section: Discussionmentioning

confidence: 96%

Mitochondrial dysfunction induced by Bisphenol A is a factor of its hepatotoxicity in rats

et al. 2015

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Bisphenol A (BPA), an estrogenic and endocrine disrupting agent, is widely used in manufacturing of polycarbonate plastics and epoxy resins. BPA and other endocrine disrupting chemicals (EDCs) act via multiple mechanisms including interference with mitochondrial functions. Mitochondria are the hub of cellular energy pool and hence are the target of many EDCs. We studied perturbation of activities of mitochondrial enzymes by BPA and its possible role in hepatotoxicity in Wistar rats. Rats were exposed to BPA (150 mg/kg, 250 mg/kg, 500 mg/kg per os, for 14 days) and activities of enzymes of mitochondrial electron transport chain (ETC) were measured. Besides, other biochemical parameters such as superoxide generation, protein oxidation, and lipid peroxidation (LPO) were also measured. Our results indicated a significant decrease in the activities of enzymes of mitochondrial ETC complexes, i.e., complex I, II, III, IV, and V along with significant increase in LPO and protein oxidation. Additionally, a significant increase in mitochondrial superoxide generation was also observed. All these findings could be attributed to enhanced oxidative stress, decrease in reduced glutathione level, and decrease in the activity of superoxide dismutase in rat liver mitochondria isolated from BPA-treated rats. BPA treatment also caused a significant increase in serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase indicating its potential hepatotoxicity. Furthermore, histopathological findings revealed marked edema formation, hepatocellular degeneration, and necrosis of liver tissue in BPA-exposed rats. In conclusion, this study provides an evidence of impaired mitochondrial bioenergetics and liver toxicity after high-dose BPA exposure in rats. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1922-1934, 2016.

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Section: Discussionmentioning

confidence: 96%

Mitochondrial dysfunction induced by Bisphenol A is a factor of its hepatotoxicity in rats

et al. 2015

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“…46,47 Microvascular processes such as those which have been identified in laboratory studies of BPA 48 that lead to low-grade albuminuria may develop over time, and so the cross-sectional association of urinary BPA with increased low-grade albuminuria does not necessarily support causation, even when consistent with growing laboratory evidence. 24,25 Even if earlier life exposures are biologically more plausible, recent evidence suggests that BPA may be stored in fat, 49–51 increasing plausibility that current urinary BPA represents earlier, or more chronic, exposures. If current uBPA is a “noisy” index of early exposure, our estimates of association should be biased towards the null.…”

Section: Discussionmentioning

confidence: 99%

“…24,25 Given that BPA is a potential contributor to physiologic processes that increase cardiometabolic risk, and since individuals with increased cardiovascular risk have increased albuminuria, 26,27 BPA exposure may be associated with low-grade albuminuria. The only study which has evaluated this possibility examined 3,055 Chinese adults living in the Shanghai region, and identified uBPA as an independent determinant of the extent of low grade albuminuria (albumin:creatinine ratio <30 mg/g), with 23% increased odds for the highest quartile of albuminuria in the highest urinary concentration BPA quartile compared to the lowest quartile.…”

Section: Introductionmentioning

confidence: 99%

Bisphenol A exposure is associated with low-grade urinary albumin excretion in children of the United States

Trasande

Attinà

Trachtman

2013

Kidney International

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Urinary bisphenol A (BPA), a widely-used biomarker of exposure to BPA, has been associated with cardiometabolic derangements in laboratory studies and with low-grade albuminuria in Chinese adults. Despite the known unique vulnerability of children to environmental chemicals, no studies have examined associations of urinary BPA with albuminuria in children. Since exposure to BPA is widespread in the United States population, we examined data from 710 children in the 2009–10 National Health and Nutrition Examination Survey with urinary BPA measurements and first morning urine samples with creatinine values. Controlled for a broad array of sociodemographic and environmental risk factors as well as insulin resistance and elevated cholesterol, children with the highest compared to the lowest quartile of urinary BPA had a significant 0.91 mg/g higher albumin-to-creatinine ratio, adjusted for the urinary BPA concentration. When the multivariable model was reprised substituting continuous measures of BPA, a significant 0.28 mg/g albumin-to-creatinine ratio increase was identified for each log unit increase in urinary BPA. Thus, an association of BPA exposure with low-grade albuminuria is consistent with previous results found in Chinese adults and documents this in children in the United States. Our findings broaden the array of adverse effects of BPA to include endothelial dysfunction as evidenced by the low-grade albuminuria and support proactive efforts to prevent harmful exposures.

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“…However, BPA (25 mg/kg) induces nephrotoxicity by increasing oxidative stress in the kidney [Korkmaz et al 2011] and causes an increase in the BUN and creatinine levels in rats treated with BPA (30 mg/kg/day) for one week [Helal et al 2013]. The BUN and creatinine ratio can be used to assess kidney injury and toxicity.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic effects of quercetin against bisphenol A induced testicular damage in male Sprague Dawley rats

Jahan

Ain

Ullah

2016

Systems Biology in Reproductive Medicine

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The present study was designed to investigate protective effects of quercetin against bisphenol A (BPA) induced testicular toxicity in male Sprague Dawley rats. Twenty adult male rats were divided into four groups. The first group served as the control and was provided with normal saline. The second group of rats was treated with 50 mg/kg of BPA dissolved in alcoholic saline. The third group received oral gavage of 50 mg/kg quercetin while the fourth group was treated with quercetin (50 mg/kg) along with BPA (50 mg/kg). All of the treatments were carried out for 52 days. Testicular tissues and epididymis were used for histology while blood plasma was used for hormonal and biochemical analysis. BPA administration resulted in a significant reduction in seminiferous tubule diameter and epithelial height with impaired spermatogenesis. Quercetin treatment resulted in restoration of spermatogenesis and reversal of histological damage. In addition, BPA treatment significantly reduced (p < 0.05) plasma testosterone level (ng/ml) while estrogen was not affected. Similarly, BPA caused a significant alteration in the lipid profile. Interestingly, quercetin treatment led to a marked increase in plasma testosterone, decrease in estrogen concentration, as well as a normalized lipid profile. In conclusion, results indicated that BPA administration induces toxic effects on testis and epididymis, impairs spermatogenesis, with an imbalance in hormonal levels and lipid profile while quercetin amended these toxic effects by restoring normal spermatogenesis, testicular tissue damage, and hormonal levels. This suggests that quercetin may be a potential therapeutic against BPA induced testicular toxicity. ARTICLE HISTORY

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Vitamin C coadministration augments bisphenol A, nonylphenol, and octylphenol induced oxidative damage on kidney of rats

Cited by 48 publications

References 44 publications

Mitochondrial dysfunction induced by Bisphenol A is a factor of its hepatotoxicity in rats

Mitochondrial dysfunction induced by Bisphenol A is a factor of its hepatotoxicity in rats

Bisphenol A exposure is associated with low-grade urinary albumin excretion in children of the United States

Therapeutic effects of quercetin against bisphenol A induced testicular damage in male Sprague Dawley rats

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