The role of DNA damage and caspase activation in cytotoxicity and genotoxicity of macrophages induced by bisphenol‐A‐glycidyldimethacrylate

Li, Y.-C.; Kuan, Yu‐Hsiang; Huang, Fu‐Mei; Chang, Yu‐Chao

doi:10.1111/j.1365-2591.2011.02001.x

Cited by 38 publications

(60 citation statements)

References 31 publications

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“…In this study, we also ascertained that the cell death patterns provoked by 0.5 mM Bis-GMA in HOK cells were mainly apoptosis. Our findings are in line with those of Chang et al (2010b) and Li et al (2012) in human dental pulp cells and murine macrophage cell line RAW264.7. However, Reichl et al (2006) have presented that Bis-GMA-induced mainly necrotic cell death in human gingival fibroblast (HGF), while apoptotic cell death events were very few.…”

Section: Discussionsupporting

confidence: 94%

N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway

Zhu

et al. 2015

Toxicology in Vitro

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Section: Discussionsupporting

confidence: 94%

N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway

Zhu

et al. 2015

Toxicology in Vitro

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“…Nevertheless, other researchers revealed that the mode of cell death due to BPA changed from apoptosis to necrosis and this was also associated with caspase activation (Li et al . ).…”

Section: Discussionmentioning

confidence: 97%

Effect of bisphenol A on morphology, apoptosis and proliferation in the resting mammary gland of the adult albino rat

Ibrahim

Elbakry

Bayomy

2016

Int J Experimental Path

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SUMMARYBisphenol A (BPA) is a synthetic oestrogen that is extensively used in a wide range of daily used plastic products. This makes it one of the environmental chemicals that may have impact on human health. Due to its oestrogenic effect, BPA might affect the mammary gland. This study aimed to investigate the influence of BPA on the histological structure of the mammary gland of the adult female albino rat and its effect on epithelial cell proliferation and apoptosis status, in addition to its possible modulating effect on estrogen receptor expression. Thirty female adult albino rats were divided into control and experimental groups. The rats in the experimental group were gavaged with 5 mg/kg BPA daily for 8 weeks. The mammary glands were dissected and processed for histological and immunohistochemical stains for Ki-67, activated caspase-3 and estrogen receptor alpha (ER-a). BPA induced an increase in the number and size of the acini and ducts in the mammary gland of treated rats with hyperplasia of their lining epithelial cells. The collagen fibre content was significantly increased in the connective tissue stroma separating the ducts. Immunohistochemical results showed a significant increase in Ki-67 and caspase-3, but a nonsignificant increase in ER-a expression. Bisphenol A induced structural changes and affected the proliferation rate of mammary glands, so it might be one of the predisposing factors for breast cancer.

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“…Pro-inflammatory cytokines and chemokines, including IL-1b, IL-6, TNF and monocyte chemoattractant protein-1 (MCP-1), are produced from hepatic macrophages in various murine models of liver injury (Tuñ on et al 2009;Zimmermann et al 2012;Shen et al 2015;Ferreira et al 2016). Furthermore, the release of these cytokines can activate macrophages during infection, injury and inflammation (Kim et al 2007;Li et al 2012). IL-1b also stimulates the production of other cytokines and recruits inflammatory cells (Tilg & Diehl 2000).…”

Section: Inflammatory Markersmentioning

confidence: 99%

Inflammation, oxidative stress and apoptosis cascade implications in bisphenol A‐induced liver fibrosis in male rats

Elswefy

Abdallah

Atteia

et al. 2016

Int J Experimental Path

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Bisphenol A (BPA) is a key monomer in the production of plastics. It has been shown to be hepatotoxic. Inflammation and oxidative stress are closely linked with liver fibrosis, the major contributing factor to hepatic failure. Therefore, the aim of this study was to evaluate the impact of chronic exposure to BPA on the development of hepatic fibrosis in male rats and to determine the cross-talk between the hepatic cytokine network, oxidative stress and apoptosis. For this purpose, 30 male Wistar albino rats were divided into three equal groups as follows: the first group was given no treatment (normal control group); the second group was given corn oil once daily by oral gavage for 8 weeks (vehicle control group); and the third group received BPA (50 mg/kg body weight/day, p.o.) for 8 weeks. BPA administration induced liver fibrosis as reflected in an increase in serum hepatic enzymes activities, hepatic hydroxyproline content and histopathological changes particularly increased collagen fibre deposition around the portal tract. In addition, there was inflammation (as reflected in increase in interleukin-1beta 'IL-1β', decrease in interleukin-10 'IL-10' serum levels and increase in IL-1β/IL-10 ratio), oxidative stress (as reflected in increase in malondialdehyde (MDA) level, reduction in reduced glutathione (GSH) content and inhibition of catalase (CAT) activity) and apoptosis [as reflected in an increase in caspase-3 level and a decrease in numbers of B-cell lymphoma 2 (BCL2)-immunopositive hepatocytes]. Interestingly, BPA had an upregulating effect on an extracellular matrix turnover gene [as reflected in matrix metalloproteinase-9 (MMP-9)] and a downregulating effect on its inhibitor gene [as reflected in tissue inhibitor of matrix metalloproteinase-2 (TIMP-2)] expression. Thus, the mechanism by which BPA induced liver fibrosis seems to be related to stimulation of the inflammatory response, along with oxidative stress, the apoptotic pathway and activation of extracellular matrix turnover.

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The role of DNA damage and caspase activation in cytotoxicity and genotoxicity of macrophages induced by bisphenol‐A‐glycidyldimethacrylate

Abstract: Cytotoxicity and genotoxicity induced by BisGMA are mediated by DNA damage and caspase activation.

Cited by 38 publications

References 31 publications

N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway

N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway

Effect of bisphenol A on morphology, apoptosis and proliferation in the resting mammary gland of the adult albino rat

Inflammation, oxidative stress and apoptosis cascade implications in bisphenol A‐induced liver fibrosis in male rats

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