Bisphenol A, bisphenol S, bisphenol F and bisphenol AF induce different oxidative stress and damage in human red blood cells ( in vitro study)

Maćczak, Aneta; Cyrkler, Monika; Bukowska, Bożena; Michałowicz, Jaromir

doi:10.1016/j.tiv.2017.02.018

Cited by 192 publications

(84 citation statements)

References 49 publications

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“…GSH‐Px is an important antioxidant enzyme widely present in the body. It can specifically catalyze the reduction reaction of GSH to H 2 O 2 , and decompose H 2 O 2 into H 2 O, which plays a role in protecting cell membrane structure and function …”

Section: Resultsmentioning

confidence: 99%

Hematological effects of ultrafine carbon black on red blood cells and hemoglobin

Pan

Zhang

et al. 2019

J Biochem & Molecular Tox

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The harmful effects of ultrafine particles (UFPs) in the atmosphere have caused widespread concern. Ultrafine carbon black (UFCB) is an important component of UFPs. In this study, we explored the impact of UFCB on the structure, the antioxidant defense system, and the ATPase activity of human red blood cells (hRBCs). It was found that UFCB decreased the activity of SOD (73.58%), CAT (89.79%), and GSH‐Px (81.02%), leading to oxidative stress in hRBCs. UFCB had no destructive effect on the structure of hRBCs in 4 hours. ATPase activity increased (119.34%) and UFCB had weakly stimulated the cell membrane. On the molecular level, spectroscopic experiments showed that bovine hemoglobin (BHb) can bind to the UFCB by electrostatic force, leading to the shrinking of the BHb skeleton and increase in microenvironment polarity. This study demonstrates the negative hematological effect of UFCB on hemoglobin and hRBCs and reveals the potential risks in animals and humans.

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Section: Resultsmentioning

confidence: 99%

Hematological effects of ultrafine carbon black on red blood cells and hemoglobin

Pan

Zhang

et al. 2019

J Biochem & Molecular Tox

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“…Moreover, administration of BPS results in necrotic, genotoxic, and neurotoxic changes . In turn, BPF induces oxidative stress and causes changes in the endocrine and reproductive systems . Based on these facts, it appears that other phenols are not safe alternatives to BPA in the production of plastics.…”

Section: Discussionmentioning

confidence: 99%

Neurochemical characterization of the enteric neurons within the porcine jejunum in physiological conditions and under the influence of bisphenol A (BPA)

Szymańska

Gonkowski

2019

Neurogastroenterology Motil

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Background Bisphenol A (BPA) is commonly used in the production of plastics and has multidirectional, negative effects on the living organisms. It may also affect the enteric nervous system (ENS) located in the wall of the gastrointestinal tract. Enteric neurons express many active substances, which regulate majority of intestinal activities not only in physiological conditions but also under the impact of pathological factors. Methods The influence of various doses of BPA on the ENS of jejunum has been investigated using the double immunofluorescence technique. The commercial antibodies against substance P (SP), vasoactive intestinal polypeptide (VIP), galanin (GAL), vesicular acetylcholine transporter (VAChT), and cocaine‐ and amphetamine‐regulated transcript peptide (CART) were used. Key Results Both doses of BPA studied changed the number of the enteric neurons immunoreactive to SP, VIP, GAL, VAChT, and CART, and the intensity of fluctuations depended on the BPA dose and on the type of the enteric plexus. Bisphenol A causes the increase in the number of neurons immunoreactive to the majority of substances studied. The only exception was VAChT‐positive neurons, the number of which was lower under the impact of BPA in the comparison with physiological conditions. Conclusions & Inferences Even low doses of BPA cause the changes in neurochemical characterization of the enteric neurons in the jejunum. These changes may be the first sign of subclinical BPA intoxication. The mechanisms of observed changes are probably connected with neurotoxic and/or pro‐inflammatory activity of BPA, but their exact mechanisms are not fully explained.

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“…Although BPA is an estrogen analog, the biologic effects that BPA exerts may differ from those of estrogen. Estrogen is seen as an antioxidant (35), whereas BPA often induces oxidative stress (36)(37)(38). The estrogen-inhibited XO activity might be explained by the antioxidant properties of estrogen (34), whereas a direct binding relationship between BPA and XO may account for the BPA-enhanced XO activity.…”

Section: Discussionmentioning

confidence: 99%

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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Bisphenol A, bisphenol S, bisphenol F and bisphenol AF induce different oxidative stress and damage in human red blood cells ( in vitro study)

Cited by 192 publications

References 49 publications

Hematological effects of ultrafine carbon black on red blood cells and hemoglobin

Hematological effects of ultrafine carbon black on red blood cells and hemoglobin

Neurochemical characterization of the enteric neurons within the porcine jejunum in physiological conditions and under the influence of bisphenol A (BPA)

Bisphenol A promotes hyperuricemia via activating xanthine oxidase

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