Bisphenol A and genistein have opposite effects on adult chicken ovary by acting on ERα/Nrf2-Keap1-signaling pathway

Gao, Zhangshan; Gao, Xiaona; Fan, Wentao; Liu, Shuhui; Li, Mengcong; Miao, Yufan; Ding, Chenchen; Tang, Zhihui; Yan, Liping; Liu, Guangliang; Shi, Xizhi; Song, Suquan

doi:10.1016/j.cbi.2021.109616

Cited by 16 publications

(9 citation statements)

References 51 publications

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“…β‐actin acted as internal reference gene. The dilution ratios of the primary antibodies were consistent with previous description: 32 Keap1 (1:500), Nrf2 (1:500), NQO1 (1:500), HO‐1 (1:500), and β‐actin (1:1000). Afterwards, the membranes were rinsed with TBST and incubated in HRP‐marked secondary antibody (1:5000) against mouse IgG at 37°C for 1 h. Ultimately, we washed the membranes and used Alliance imager Q9 (UVITEC, UK) and the ECL chemiluminescence reagent observe positive fluorescence signal.…”

Section: Methodssupporting

confidence: 85%

Bromoacetic acid causes oxidative stress and uric acid metabolism dysfunction via disturbing mitochondrial function and Nrf2 pathway in chicken kidney

Liu

et al. 2022

Environmental Toxicology

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Since the outbreak of COVID‐19, widespread utilization of disinfectants has led to a tremendous increase in the generation of disinfection byproducts worldwide. Bromoacetic acid (BAA), one of the common disinfection byproducts in the environment, has triggered public concern because of its adverse effects on urinary system in mammals. Nevertheless, the BAA‐induced nephrotoxicity and potential mechanism in birds still remains obscure. According to the detected content in the Taihu Lake Basin, the model of BAA exposure in chicken was established at doses of 0, 3, 300, 3000 μg/L for 4 weeks. Our results indicated that BAA exposure caused kidney swelling and structural disarrangement. BAA led to disorder in renal function (CRE, BUN, UA) and increased apoptosis (Bax, Bcl‐2, caspase3). BAA suppressed the expression of mitochondrial biogenesis genes (PGC‐1α, Nrf1, TFAM) and OXPHOS complex I genes (ND1, ND2, ND3, ND4, ND4L, ND5, ND6). Subsequently, BAA destroyed the expression of Nrf2 antioxidant reaction genes (Nrf2, Keap1, HO‐1, NQO1, GCLM, GCLC). Furthermore, renal oxidative damage led to disorder in uric acid metabolism genes (Mrp2, Mrp4, Bcrp, OAT1, OAT2, OAT3) and exacerbated destruction in renal function. Overall, our study provided insights into the potential mechanism of BAA‐induced nephrotoxicity, which were important for the clinical monitoring and prevention of BAA.

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Section: Methodssupporting

confidence: 85%

Bromoacetic acid causes oxidative stress and uric acid metabolism dysfunction via disturbing mitochondrial function and Nrf2 pathway in chicken kidney

Liu

et al. 2022

Environmental Toxicology

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“…Additionally, exposure to BPA and genistein alters the expression of the estrogen receptor alpha (ERα) in the ovary. The use of a specific ERα agonist/antagonist confirmed that BPA and genistein have opposite regulatory effects on the Nrf2-Keap1 pathway by targeting Erα [ 95 ].…”

Section: Survey Of Antioxidants That Affected Bpa Toxicitymentioning

confidence: 99%

Can Antioxidants Reduce the Toxicity of Bisphenol?

2022

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BPA is still the subject of extensive research due to its widespread use, despite its significant toxicity resulting not only from its negative impact on the endocrine system but also from disrupting the organism’s oxidative homeostasis. At the molecular level, bisphenol A (BPA) causes an increased production of ROS and hence a change in the redox balance, mitochondrial dysfunction, and modulation of cell signaling pathways. Importantly, these changes accumulate in animals and humans, and BPA toxicity may be aggravated by poor diet, metabolic disorders, and coexisting diseases. Accordingly, approaches using antioxidants to counteract the negative effects of BPA are being considered. The preliminary results that are described in this paper are promising, however, it should be emphasized that further studies are required to determine the optimal dosage and treatment regimen to counteract BPA toxicity. It also seems necessary to have a more holistic approach showing, on the one hand, the influence of BPA on the overall human metabolism and, on the other hand, the influence of antioxidants in doses that are acceptable with the diet on BPA toxicity. This is due in part to the fact that in many cases, the positive effect of antioxidants in in vitro studies is not confirmed by clinical studies. For this reason, further research into the molecular mechanisms of BPA activity is also recommended.

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“…The ability of quercetin, genistein, and procyanidin B2 to activate the Nrf2/ARE pathway has been previously demonstrated in numerous experimental models [ 63 , 64 , 65 , 66 , 67 ]. In this study, both quercetin and genistein treatments alone did not increase the p-Nrf2/Nrf2 ratio in BEAS-2B cells significantly ( p > 0.05).…”

Section: Discussionmentioning

confidence: 99%

Genistein and Procyanidin B2 Reduce Carcinogen-Induced Reactive Oxygen Species and DNA Damage through the Activation of Nrf2/ARE Cell Signaling in Bronchial Epithelial Cells In Vitro

Suraweera

Merlin

Dellaire

et al. 2023

IJMS

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Cancer is one of the leading causes of death worldwide. Chemotherapy and radiation therapy are currently providing the basis for cancer therapies, although both are associated with significant side effects. Thus, cancer prevention through dietary modifications has been receiving growing interest. The potential of selected flavonoids in reducing carcinogen-induced reactive oxygen species (ROS) and DNA damage through the activation of nuclear factor erythroid 2 p45 (NF-E2)-related factor (Nrf2)/antioxidant response element (ARE) pathway was studied in vitro. Dose-dependent effects of pre-incubated flavonoids on pro-carcinogen 4-[(acetoxymethyl)nitrosamino]-1-(3-pyridyl)-1-butanone (NNKAc)-induced ROS and DNA damage in human bronchial epithelial cells were studied in comparison to non-flavonoids. The most effective flavonoids were assessed for the activation of Nrf2/ARE pathway. Genistein, procyanidin B2 (PCB2), and quercetin significantly suppressed the NNKAc-induced ROS and DNA damage. Quercetin significantly upregulated the phosphorylated protein kinase B/Akt. PCB2 significantly upregulated the activation of Nrf2 and Akt through phosphorylation. Genistein and PCB2 significantly upregulated the phospho-Nrf2 nuclear translocation and catalase activity. In summary, genistein and PCB2 reduced the NNKAc-induced ROS and DNA damage through the activation of Nrf2. Further studies are required to understand the role of dietary flavonoids on the regulation of the Nrf2/ARE pathway in relation to carcinogenesis.

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Bisphenol A and genistein have opposite effects on adult chicken ovary by acting on ERα/Nrf2-Keap1-signaling pathway

Cited by 16 publications

References 51 publications

Bromoacetic acid causes oxidative stress and uric acid metabolism dysfunction via disturbing mitochondrial function and Nrf2 pathway in chicken kidney

Bromoacetic acid causes oxidative stress and uric acid metabolism dysfunction via disturbing mitochondrial function and Nrf2 pathway in chicken kidney

Can Antioxidants Reduce the Toxicity of Bisphenol?

Genistein and Procyanidin B2 Reduce Carcinogen-Induced Reactive Oxygen Species and DNA Damage through the Activation of Nrf2/ARE Cell Signaling in Bronchial Epithelial Cells In Vitro

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