Nonylphenol diethoxylate inhibits apoptosis induced in <scp>PC</scp>12 cells

Liu, Chuang; Sun, Yangying; Song, Yutong; Saito, Takeshi; Kurasaki, Masaaki

doi:10.1002/tox.22144

Cited by 3 publications

(3 citation statements)

References 45 publications

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“…Our data reporting an enhanced survival to STS-induced apoptosis in MCF-10A are in line with inhibition of induced cell death by BPA or nonylphenol reported in rat PC12, hippocampal, and neuronal cells ( 42 , 43 ). Another consequence of alkylphenol exposure was the stimulation of migratory potential as supported by enhanced wound filling and EMT marker expression.…”

Section: Discussionsupporting

confidence: 91%

Low-Dose Alkylphenol Exposure Promotes Mammary Epithelium Alterations and Transgenerational Developmental Defects, But Does Not Enhance Tumorigenic Behavior of Breast Cancer Cells

et al. 2017

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Fetal and neonatal exposure to long-chain alkylphenols has been suspected to promote breast developmental disorders and consequently to increase breast cancer risk. However, disease predisposition from developmental exposures remains unclear. In this work, human MCF-10A mammary epithelial cells were exposed in vitro to a low dose of a realistic (4-nonylphenol + 4-tert-octylphenol) mixture. Transcriptome and cell-phenotype analyses combined to functional and signaling network modeling indicated that long-chain alkylphenols triggered enhanced proliferation, migration ability, and apoptosis resistance and shed light on the underlying molecular mechanisms which involved the human estrogen receptor alpha 36 (ERα36) variant. A male mouse-inherited transgenerational model of exposure to three environmentally relevant doses of the alkylphenol mix was set up in order to determine whether and how it would impact on mammary gland architecture. Mammary glands from F3 progeny obtained after intrabuccal chronic exposure of C57BL/6J P0 pregnant mice followed by F1–F3 male inheritance displayed an altered histology which correlated with the phenotypes observed in vitro in human mammary epithelial cells. Since cellular phenotypes are similar in vivo and in vitro and involve the unique ERα36 human variant, such consequences of alkylphenol exposure could be extrapolated from mouse model to human. However, transient alkylphenol treatments combined to ERα36 overexpression in mammary epithelial cells were not sufficient to trigger tumorigenesis in xenografted Nude mice. Therefore, it remains to be determined if low-dose alkylphenol transgenerational exposure and subsequent abnormal mammary gland development could account for an increased breast cancer susceptibility.

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Section: Discussionsupporting

confidence: 91%

Low-Dose Alkylphenol Exposure Promotes Mammary Epithelium Alterations and Transgenerational Developmental Defects, But Does Not Enhance Tumorigenic Behavior of Breast Cancer Cells

et al. 2017

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“…A previous study indicated that CRC was an estrogen-dependent tumor type, and the level of estrogen in patients was directly associated with the development and prognosis of CRC (2). NP is an EDC, which has the ability to induce endocrine disruption, reproduction disorders and the development of various types of cancer (20)(21)(22)(23).…”

Section: Discussionmentioning

confidence: 99%

Nonylphenol promotes the proliferation of colorectal cancer COLO205 cells by upregulating the expression of protein kinase C ζ

et al. 2018

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Previous studies have indicated the potential role of estrogen in the development and prognosis of colorectal cancer (CRC). Nonylpheno (NP) is an endocrine-disrupting chemical, which may inf luence the development of estrogen-dependent types of cancer. However, the molecular mechanism of NP in the development of CRCs remains unclear. In the present study, various concentrations of NP were used to treat COLO205 CRC cells, and the expression of protein kinase C ζ (PKCζ) was knocked down using PKCζ small interfering RNA. The effects of NP in various concentrations on the cell cycle and apoptosis of COLO205 cells were examined, and the change in the expression level of PKCζ was analyzed. The results indicated that NP may significantly induce proliferation of COLO205 CRC cells, and significantly reduce cell apoptosis. However, suppression of PKCζ expression may inhibit proliferation, while NP could reduce this inhibition. The results of a western blot analysis indicated that the expression level of cyclin D1 and E were significantly increased following NP treatment, and the expression of p27 was significantly decreased. The phosphorylation of PKCζ and extracellular-signal-regulated kinase (ERK)1/2 was significantly increased following NP treatment in a dose-dependent manner. Overall, NP induced human CRC COLO205 cell proliferation and inhibited the apoptotic rate of COLO205 cells by increasing the activity of PKCζ and ERK1/2.

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“…The results of Yu et al 4 showed that NP, due to its lipolytic nature, can embed and accumulate in cell membranes and reduce the Ca 2+ pump activity on the cell membrane. NP also can enhance serum deprivation to induce apoptosis in PC12 cells, 5 inhibit the tumor‐preventive function of lymphocytes and macrophages by affecting their immune response, 6 and also induce pancreatic cell damage in rats through mitochondrial dysfunction and oxidative stress 7 . Taken together, NP can lead to disruption of metabolic homeostasis, cellular damage, and organ toxicity through multiple pathways.…”

Section: Introductionmentioning

confidence: 99%

Curative effect of zinc‐selenium tea on rat's cardiotoxicity induced by long‐term exposure to nonylphenol

Zhang

Liu

et al. 2022

Environmental Toxicology

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This study aimed to explore whether zinc‐selenium tea has an curative effect on the cardiotoxicity induced by nonylphenol (NP), and to compare the effect of zinc‐selenium tea and green tea. After drinking of zinc‐selenium tea or green tea, compared with the control group, the left ventricular anterior wall became thinner, and the left ventricular end‐diastolic diameter increased, the anterior wall of the left ventricle became thin at the end of diastole in the NP group. The serum myocardial enzymes aspartate aminotransferase, creatine kinase, creatine kinase isoenzyme, lactate dehydrogenase, and α‐hydroxybutyrate dehydrogenase in the NP group were significantly increased, and the serum myocardial enzymes were significantly decreased after the intervention of zinc‐selenium tea. Proteins and mRNA expressions of Collagen I and Collagen III in the tea groups were lower than those in the NP group. In the green tea and zinc‐selenium tea intervention groups, the disorder and degree of myocardial fiber were alleviated to varying degrees. The disturbance, breakage, and inflammatory cell infiltration of myocardial fibers in zinc‐selenium tea and green tea groups were less than that of NP group. After tea intervention, collagen I and collagen III in the myocardium decreased. The intervention effect of zinc‐selenium tea was better than that of green tea. Zinc‐selenium tea and green tea could interfere with the cardiotoxicity indued by NP, which would alleviate the myocardial fibrosis by reducing expressions of collagen I and collagen III. Moreover, the curative effect of zinc‐selenium tea was better than that of green tea.

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Nonylphenol diethoxylate inhibits apoptosis induced in PC12 cells

Cited by 3 publications

References 45 publications

Low-Dose Alkylphenol Exposure Promotes Mammary Epithelium Alterations and Transgenerational Developmental Defects, But Does Not Enhance Tumorigenic Behavior of Breast Cancer Cells

Low-Dose Alkylphenol Exposure Promotes Mammary Epithelium Alterations and Transgenerational Developmental Defects, But Does Not Enhance Tumorigenic Behavior of Breast Cancer Cells

Nonylphenol promotes the proliferation of colorectal cancer COLO205 cells by upregulating the expression of protein kinase C ζ

Curative effect of zinc‐selenium tea on rat's cardiotoxicity induced by long‐term exposure to nonylphenol

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