Bisphenol A Induces Apoptosis in Liver Cells through Induction of ROS

Kourouma, Ansoumane; Quan, Chao; Duan, Peng; Qi, Suqin; Yu, Tingting; Wang, Yinan; Yang, Kecheng

doi:10.1155/2015/901983

Cited by 46 publications

(32 citation statements)

References 44 publications

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“…Another explanation could be the fact that BPA-induced liver damage was so severe that corn oil coadministration failed to reduce such damage to approach the control group. In concordance, previous studies indicated BPA induced deleterious effects on the liver and other organs even it was dissolved in corn oil (El Ghazzawy et al 2011;Yıldız & Barlas 2013;Kourouma et al 2015;Kazemi et al 2016).…”

Section: Discussionsupporting

confidence: 90%

“…Because GSH is an important cofactor for GPx activity (Huang et al 2004), reduction in hepatic GSH content here may reduce GPx activity enhancing oxidative stress. This may be attributed to BPA-induced oxidative damage to the liver releasing hepatic enzymes into the blood or to hyperactivity of the liver (Kourouma et al 2015). Thus, exposure to BPA in the current study might increase the activity of GST to help in the detoxification of BPA and degradation of lipid peroxides at the expense of GSH content that participates in the catalytic activity of GST.…”

Section: Inflammatory Markersmentioning

confidence: 83%

“…In addition, both ALT and AST activities were increased significantly following BPA administration. This may be attributed to BPA-induced oxidative damage to the liver releasing hepatic enzymes into the blood or to hyperactivity of the liver (Kourouma et al 2015). In consistence, inflammatory response to BPA administration might be involved in BPA-induced liver damage here because hepatic enzyme activities are strongly and positively correlated with the pro-inflammatory cytokine (IL-1b) level and IL-1b/IL-10 ratio.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 90%

Section: Inflammatory Markersmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

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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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“…In agreement to our results, a significant increase in the serum MDA level were found in rats exposed to BPA compared to the control group [16] . Also, study of Kourouma et al [17] showed exposure of rats to BPA resulted in significant increase of liver MDA level. Several studies [2,3,12,13,18,19] demonstrated that exposure to BPA generate reactive oxygen species, but reduce antioxidant content and activity.…”

Section: Discussionmentioning

confidence: 95%

Bisfenol A’ya Maruz Bırakılmış Sıçanlarda İmmun Hücre sayısı, Plazma İmmunglobulin İçeriği ve INF-γ Gen Ekspresyonu

Elhami¹,

Sadeghi²

2016

Kafkas Univ Vet Fak Derg

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The purpose of this study was to evaluate the effect of low-dose graded of bisphenol A (BPA) on immune cell counts, immunoglobulin contents and gamma-interferon (INF-γ) gene expression in rats. Bisphenol A was injected intraperitoneally to male Wistar rats at doses of 15, 30 and 45 µg/kg body weight for 5 weeks. Rats were anesthetized with diethyl ether and blood samples collected, plasma separated and spleen inserted in liquid nitrogen. Total and differential white blood cells, antibody titers, and gene expression of INF-γ were measured. Plasma malondialdehyde levels increased linearly as BPA doses increased. Bisphenol A at dose of 45 µg/kg body weight resulted in significant increase of plasma cortisol level as compared with other treatments. Red blood cell counts decreased linearly as doses of BPA increased. There were no significant differences among treatment for eosinophil, monocytes and basophil counts. The gene expression of INF-γ increased as doses of BPA increased. Rats received 45 µg BPA/kg body weight had 3.2 folds higher gene expression of INF-γ than the control group. The plasma IgG and IgA levels increased linearly as bisphenol doses increased. There was no significant difference among treatments for plasma IgM level. Based on the results of this study, BPA at low doses may result in increase of immune responses in a dose dependent manner. Keywords: bisphenol A, Blood cells counts, INF-γ, Immune response, Rat Bisfenol A'ya Maruz Bırakılmış Sıçanlarda İmmun Hücre Sayısı, Plazma İmmunglobulin İçeriği ve INF-γ Gen Ekspresyonu ÖzetBu çalışmanın amacı, sıçanlarda immun hücre sayısı, immunoglobulin içeriği ve gama-interferon (INF-γ) gen ekspresyonu üzerine bisfenol A'nın (BPA) kademeli düşük doz etkisini değerlendirmekti. Bisfenol A Erkek Wistar ratlara 5 hafta boyunca 15, 30 ve 45 ug/kg canlı ağırlık (c.a.) dozlarında intraperitonal olarak enjekte edildi. Sıçanlar dietil eter ile anestetize sonra kan örnekleri toplandı, plazma ayrıldı ve dalak sıvı azot içine konuldu. Toplam ve diferansiyel beyaz kan hücreleri, antikor titreleri, ve INF-y gen ekspresyonu ölçüldü. Plazma malondialdehit düzeyleri BPA dozları arttıkça doğrusal olarak arttı. Bisfenol A'nın 45 ug/kg c.a. dozu, diğer tedaviler ile karşılaştırıldığında plazma kortizol seviyesinde önemli bir artışla sonuçlandı. BPA dozları arttıkça kırmızı kan hücresi sayımları da doğrusal azaldı. Tedavi grupları arasında eozinofil, monosit ve bazofil sayıları yönünden anlamlı bir fark saptanmadı. BPA dozları arttıkça INF-y gen ekpresyonu da arttı. 45ug/kg c.a. BPA verilen sıçanlar kontrol grubuna göre 3.2 kat daha yüksek INF-y gen ekpresyonuna sahipti. Plazma IgG ve IgA düzeyleri bisfenol dozları arttıkça doğrusal olarak arttı. Plazma IgM düzeyi için tedavi grupları arasında anlamlı bir fark yoktu. Bu çalışmanın sonuçlarına göre; düşük dozlardaki BPA, doz-bağımlı bir şekilde immun tepkilerin artmasına neden olabilir.

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“…Previous studies have proposed that the increase in lipid peroxidation is directly proportional to that of LDH activity (Hrelia et al, 2002) in the extracellular fluid, hence indicating myocardial cell membrane damage. Elevation of LDH activity usually denotes irreversible cardiomyocyte injury (Kourouma et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

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Background: Oxidative stress plays an important role in the pathogenesis of heart diseases. Antioxidants such as palm tocotrienol-rich fraction (TRF) can reduce oxidative stress, hence preventing and reducing the risk of heart disease. This study was aimed to determine the protective effects of TRF against hydrogen peroxide (H 2 O 2)-induced oxidative stress in neonatal rat cardiomyocytes (NRCM). Methods: The NRCM were divided into five groups: (1) control, (2) cells treated with TRF (10 µg/ml) for 24 hours, (3) cells subjected to H 2 O 2 (0.5 mM) for 30 minutes, (4) cells pre-treated with TRF, and (5) cells post-treated with TRF. The IC 50 of H 2 O 2 (0-5 mM) and the effective dose of TRF (0-25 µg/ml) were determined using the MTS cell viability assay. Meanwhile, ELISA was used to measure the level of reactive oxygen species (ROS). The presence of superoxides and H 2 O 2 were detected by dihydroethidium and 5-(and-6)-carboxy-2′,7′dichlorodihydrofluorescein diacetate respectively. Flowcytometry analysis was conducted to determine the presence of apoptosis and measure the mitochondrial membrane potential, whereby the former involved the use of Annexin V-FITC stain while the latter JC-1 stain. The gene expressions of antioxidant (SOD, CAT, GPx) and apoptosis (Bax, Bcl-2, Caspase-3) enzymes were studied using qRT-PCR. Results: The IC 50 of H 2 O 2 was 0.5 mM while the effective dose of TRF 10 µg/ml. The cells which were subjected to H 2 O 2 showed a decrease in NRCM viability and significant increase (p < 0.05) in ROS production. LDH activity and green fluorescence intensity (which indicated mitochondrial depolarisation) were increased following H 2 O 2 induction. With reference to the control, the H 2 O 2-induced group had a higher percentage of late apoptotic cells, which was associated with the upregulation of the pro-apoptotic gene, Bax, and downregulation of the anti-apoptotic gene, Bcl-2 (p < 0.05). H 2 O 2 also upregulated GPx expression , apart from downregulating CAT and Cu/Zn SOD expression (p < 0.05). The pre-and post-treatment groups had increased cell viability and reduced ROS production. Pre-treatment with TRF protected the cell membranes and mitochondria from H 2 O 2-induced injury, as reflected by the reduction in extracellular LDH activity and apoptosis (the latter of which was associated with the

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Bisphenol A Induces Apoptosis in Liver Cells through Induction of ROS

Cited by 46 publications

References 44 publications

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

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

Bisfenol A’ya Maruz Bırakılmış Sıçanlarda İmmun Hücre sayısı, Plazma İmmunglobulin İçeriği ve INF-γ Gen Ekspresyonu

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