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Ming-yung Chou – One of the best experts on this subject based on the ideXlab platform.

  • Cytotoxic and non‐genotoxic effects of Arecoline on human buccal fibroblasts in vitro
    Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pat, 2007
    Co-Authors: Yu-chao Chang, Kuo-wei Tai, Min-hsiung Cheng, Lin Shin-shen Chou, Ming-yung Chou

    Abstract:

    Chang YC, Tai KW, Cheng MH, Chou LSS, Chou MY: Cytotoxic and non-genotoxic effects of Arecoline on human buccal fibroblasts in vitro. J Oral Pathol Med 1998; 27: 68–71. © Munksgaard, 1998.

    Betel quid chewing has been linked to oral submucous fibrosis and oral cancer. Cytotoxicity and genotoxicity assays were used to investigate the pathobiologi-cal effects of Arecoline on cultured human buccal fibroblasts. Arecoline increased double-stranded polynucleic acid at the concentration of 0.1 to 10 μg/ml in a concentration-dependent manner. At a concentration higher than 50 μg/ml, Arecoline was cytotoxic to cultured fibroblasts and the cytotoxicity was dose-dependent. No genotoxicity for Arecoline was found even at a concentration of 400 μg/ml. On the other hand, 600 μg/ml glutathione (GSH) and 200 μg/ml glycyrrhizin could prevent the Arecoline-induced cytotoxicity. These results indicate that Arecoline is a cytotoxic agent and no genotoxicity was found to human buccal fibroblasts. Furthermore, increasing consumption of GSH- and glycyrrhizin-rich foods may reduce the oral diseases associated with betel quid chewing.

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  • cytotoxic and non genotoxic effects of Arecoline on human buccal fibroblasts in vitro
    Journal of Oral Pathology & Medicine, 2007
    Co-Authors: Yu-chao Chang, Kuo-wei Tai, Min-hsiung Cheng, Lin Shin-shen Chou, Ming-yung Chou

    Abstract:

    Chang YC, Tai KW, Cheng MH, Chou LSS, Chou MY: Cytotoxic and non-genotoxic effects of Arecoline on human buccal fibroblasts in vitro. J Oral Pathol Med 1998; 27: 68–71. © Munksgaard, 1998.

    Betel quid chewing has been linked to oral submucous fibrosis and oral cancer. Cytotoxicity and genotoxicity assays were used to investigate the pathobiologi-cal effects of Arecoline on cultured human buccal fibroblasts. Arecoline increased double-stranded polynucleic acid at the concentration of 0.1 to 10 μg/ml in a concentration-dependent manner. At a concentration higher than 50 μg/ml, Arecoline was cytotoxic to cultured fibroblasts and the cytotoxicity was dose-dependent. No genotoxicity for Arecoline was found even at a concentration of 400 μg/ml. On the other hand, 600 μg/ml glutathione (GSH) and 200 μg/ml glycyrrhizin could prevent the Arecoline-induced cytotoxicity. These results indicate that Arecoline is a cytotoxic agent and no genotoxicity was found to human buccal fibroblasts. Furthermore, increasing consumption of GSH- and glycyrrhizin-rich foods may reduce the oral diseases associated with betel quid chewing.

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  • elevated vimentin expression in buccal mucosal fibroblasts by Arecoline in vitro as a possible pathogenesis for oral submucous fibrosis
    Oral Oncology, 2002
    Co-Authors: Yu-chao Chang, Ming-yung Chou, Kuo-wei Tai, Chung-hung Tsai, S F Yang, Chong-kuei Lii

    Abstract:

    Areca quid chewing is strongly correlated with oral submucous fibrosis (OSF) in Taiwan. The cytotoxicity of Arecoline, a major areca nut alkaloid, on human oral fibroblasts has been extensively studied. To date, however, there has been little research exploring the possible effects of Arecoline on cytoskeleton components. In this study, in addition to conducting a cytotoxicity assay, we examine the effect of Arecoline on vimentin, an intermediate filament, and its expression in human buccal mucosal fibroblasts on exposure to various levels of Arecoline (0–200 μg/ml) for 48 h. At a concentration above 50 μg/ml, Arecoline demonstrated dose-dependent cytotoxicity (P<0.05) for cultured fibroblasts. Using sodium dodecyl sulphate-polyacrylamide gel electrophoresis, we demonstrated dose-dependent elevation of 57 kDa cytoskeletal-protein levels for Arecoline. Evidence from immunoblotting assay indicated this 57 kDa cytoskeletal protein was vimentin. The increase in vimentin with Arecoline exposure corresponded to that noted for fibroblasts cultured from OSF patients. Immunohistochemical assay also revealed that vimentin expression was much higher for OSF specimens than for normal buccal mucosa. We suggest these results may advance understanding of the possible pathogenesis for submucous fibrosis through the transformation of normal buccal mucosa as a result of areca quid chewing.

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Lea-yea Chuang – One of the best experts on this subject based on the ideXlab platform.

  • Arecoline induced phosphorylated p53 and p21 waf1 protein expression is dependent on atm atr and phosphatidylinositol 3 kinase in clone 9 cells
    Journal of Cellular Biochemistry, 2009
    Co-Authors: Wen-wen Chou, Jinn-yuh Guh, Jung-fa Tsai, Chi-ching Hwang, Sheanjaw Chiou, Lea-yea Chuang

    Abstract:

    Betel-quid use is associated with liver cancer whereas its constituent Arecoline is cytotoxic, genotoxic, and induces p53-dependent p21(WAF1) protein expression in Clone-9 cells (rat hepatocytes). The ataxia telangiectasia mutated (ATM)/rad3-related (ATR)-p53-p21(WAF1) and the phosphatidylinositol-3-kinase (PI3K)-mammalian target of rapamycin (mTOR) pathways are involved in the DNA damage response and the pathogenesis of cancers. Thus, we studied the role of ATM/ATR and PI3K in Arecoline-induced p53 and p21(WAF1) protein expression in Clone-9 cells. We found that Arecoline (0.5 mM) activated the ATM/ATR kinase at 30 min. The Arecoline-activated ATM/ATR substrate contained p-p53Ser15. Moreover, Arecoline only increased the levels of the p-p53Ser6, p-p53Ser15, and p-p53Ser392 phosphorylated p53 isoforms among the known isoforms. ATM shRNA attenuated Arecoline-induced p-p53Ser15 and p21(WAF1) at 24 h. Arecoline (0.5 mM) increased phosphorylation levels of p-AktSer473 and p-mTORSer2448 at 30-60 min. Dominant-negative PI3K plasmids attenuated Arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated Arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated Arecoline-induced p21(WAF1) gene transcription. We conclude that Arecoline activates the ATM/ATR-p53-p21(WAF1) and the PI3K/Akt-mTOR-p53 pathways in Clone-9 cells. Arecoline-induced phosphorylated p-p53Ser15 expression is dependent on ATM whereas Arecoline-induced p21(WAF1) protein expression is dependent on ATM and PI3K. Moreover, p21(WAF1) gene is transcriptionally induced by Arecoline-activated ATM.

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  • Arecoline-induced growth arrest and p21WAF1 expression are dependent on p53 in rat hepatocytes.
    Toxicology, 2007
    Co-Authors: Wen-wen Chou, Jinn-yuh Guh, Jung-fa Tsai, Chi-ching Hwang, Hung-chun Chen, Jau-shyang Huang, Yu-lin Yang, Wen-chun Hung, Lea-yea Chuang

    Abstract:

    Betel-quid use is associated with the risk of liver cirrhosis and hepatocellular carcinoma and Arecoline, the major alkaloid of betel-quid, is hepatotoxic in mice. Therefore, we studied the cytotoxic and genotoxic effects of Arecoline in normal rat hepatocytes (Clone-9 cells). Arecoline dose-dependently (0.1-1mM) decreased cell cycle-dependent proliferation while inducing DNA damage at 24h. Moreover, Arecoline (1mM)-induced apoptosis and necrosis at 24h. Arecoline dose-dependently (0.1-0.5mM) increased transforming growth factor-beta (TGF-beta) mRNA, gene transcription and bioactivity and neutralizing TGF-beta antibody attenuated Arecoline (0.5mM)-inhibited cell proliferation at 24h. Arecoline (0.5mM) also increased p21(WAF1) protein expression and p21(WAF1) gene transcription. Moreover, Arecoline (0.5mM) time-dependently (8-24h) increased p53 serine 15 phosphorylation. Pifithrin-alpha (p53 inhibitor) and the loss of the two p53-binding elements in the p21(WAF1) gene promoter attenuated Arecoline-induced p21(WAF1) gene transcription at 24h. Pifithrin-alpha also attenuated Arecoline (0.5mM)-inhibited cell proliferation at 24h. We concluded that Arecoline induces cytotoxicity, DNA damage, G(0)/G(1) cell cycle arrest, TGF-beta1, p21(WAF1) and activates p53 in Clone-9 cells. Moreover, Arecoline-induced p21(WAF1) is dependent on p53 while Arecoline-inhibited growth is dependent on both TGF-beta and p53.

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  • Arecoline-induced growth arrest and p21WAF1 expression are dependent on p53 in rat hepatocytes.
    Toxicology, 2007
    Co-Authors: Wen-wen Chou, Jinn-yuh Guh, Jung-fa Tsai, Chi-ching Hwang, Hung-chun Chen, Jau-shyang Huang, Yu-lin Yang, Wen-chun Hung, Lea-yea Chuang

    Abstract:

    Abstract Betel-quid use is associated with the risk of liver cirrhosis and hepatocellular carcinoma and Arecoline, the major alkaloid of betel-quid, is hepatotoxic in mice. Therefore, we studied the cytotoxic and genotoxic effects of Arecoline in normal rat hepatocytes (Clone-9 cells). Arecoline dose-dependently (0.1–1 mM) decreased cell cycle-dependent proliferation while inducing DNA damage at 24 h. Moreover, Arecoline (1 mM)-induced apoptosis and necrosis at 24 h. Arecoline dose-dependently (0.1–0.5 mM) increased transforming growth factor-β (TGF-β) mRNA, gene transcription and bioactivity and neutralizing TGF-β antibody attenuated Arecoline (0.5 mM)-inhibited cell proliferation at 24 h. Arecoline (0.5 mM) also increased p21 WAF1 protein expression and p21 WAF1 gene transcription. Moreover, Arecoline (0.5 mM) time-dependently (8–24 h) increased p53 serine 15 phosphorylation. Pifithrin-α (p53 inhibitor) and the loss of the two p53-binding elements in the p21 WAF1 gene promoter attenuated Arecoline-induced p21 WAF1 gene transcription at 24 h. Pifithrin-α also attenuated Arecoline (0.5 mM)-inhibited cell proliferation at 24 h. We concluded that Arecoline induces cytotoxicity, DNA damage, G 0 /G 1 cell cycle arrest, TGF-β1, p21 WAF1 and activates p53 in Clone-9 cells. Moreover, Arecoline-induced p21 WAF1 is dependent on p53 while Arecoline-inhibited growth is dependent on both TGF-β and p53.

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Yu-chao Chang – One of the best experts on this subject based on the ideXlab platform.

  • Cytotoxic and non‐genotoxic effects of Arecoline on human buccal fibroblasts in vitro
    Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pat, 2007
    Co-Authors: Yu-chao Chang, Kuo-wei Tai, Min-hsiung Cheng, Lin Shin-shen Chou, Ming-yung Chou

    Abstract:

    Chang YC, Tai KW, Cheng MH, Chou LSS, Chou MY: Cytotoxic and non-genotoxic effects of Arecoline on human buccal fibroblasts in vitro. J Oral Pathol Med 1998; 27: 68–71. © Munksgaard, 1998.

    Betel quid chewing has been linked to oral submucous fibrosis and oral cancer. Cytotoxicity and genotoxicity assays were used to investigate the pathobiologi-cal effects of Arecoline on cultured human buccal fibroblasts. Arecoline increased double-stranded polynucleic acid at the concentration of 0.1 to 10 μg/ml in a concentration-dependent manner. At a concentration higher than 50 μg/ml, Arecoline was cytotoxic to cultured fibroblasts and the cytotoxicity was dose-dependent. No genotoxicity for Arecoline was found even at a concentration of 400 μg/ml. On the other hand, 600 μg/ml glutathione (GSH) and 200 μg/ml glycyrrhizin could prevent the Arecoline-induced cytotoxicity. These results indicate that Arecoline is a cytotoxic agent and no genotoxicity was found to human buccal fibroblasts. Furthermore, increasing consumption of GSH- and glycyrrhizin-rich foods may reduce the oral diseases associated with betel quid chewing.

    Free Register to Access Article

  • cytotoxic and non genotoxic effects of Arecoline on human buccal fibroblasts in vitro
    Journal of Oral Pathology & Medicine, 2007
    Co-Authors: Yu-chao Chang, Kuo-wei Tai, Min-hsiung Cheng, Lin Shin-shen Chou, Ming-yung Chou

    Abstract:

    Chang YC, Tai KW, Cheng MH, Chou LSS, Chou MY: Cytotoxic and non-genotoxic effects of Arecoline on human buccal fibroblasts in vitro. J Oral Pathol Med 1998; 27: 68–71. © Munksgaard, 1998.

    Betel quid chewing has been linked to oral submucous fibrosis and oral cancer. Cytotoxicity and genotoxicity assays were used to investigate the pathobiologi-cal effects of Arecoline on cultured human buccal fibroblasts. Arecoline increased double-stranded polynucleic acid at the concentration of 0.1 to 10 μg/ml in a concentration-dependent manner. At a concentration higher than 50 μg/ml, Arecoline was cytotoxic to cultured fibroblasts and the cytotoxicity was dose-dependent. No genotoxicity for Arecoline was found even at a concentration of 400 μg/ml. On the other hand, 600 μg/ml glutathione (GSH) and 200 μg/ml glycyrrhizin could prevent the Arecoline-induced cytotoxicity. These results indicate that Arecoline is a cytotoxic agent and no genotoxicity was found to human buccal fibroblasts. Furthermore, increasing consumption of GSH- and glycyrrhizin-rich foods may reduce the oral diseases associated with betel quid chewing.

    Free Register to Access Article

  • elevated vimentin expression in buccal mucosal fibroblasts by Arecoline in vitro as a possible pathogenesis for oral submucous fibrosis
    Oral Oncology, 2002
    Co-Authors: Yu-chao Chang, Ming-yung Chou, Kuo-wei Tai, Chung-hung Tsai, S F Yang, Chong-kuei Lii

    Abstract:

    Areca quid chewing is strongly correlated with oral submucous fibrosis (OSF) in Taiwan. The cytotoxicity of Arecoline, a major areca nut alkaloid, on human oral fibroblasts has been extensively studied. To date, however, there has been little research exploring the possible effects of Arecoline on cytoskeleton components. In this study, in addition to conducting a cytotoxicity assay, we examine the effect of Arecoline on vimentin, an intermediate filament, and its expression in human buccal mucosal fibroblasts on exposure to various levels of Arecoline (0–200 μg/ml) for 48 h. At a concentration above 50 μg/ml, Arecoline demonstrated dose-dependent cytotoxicity (P<0.05) for cultured fibroblasts. Using sodium dodecyl sulphate-polyacrylamide gel electrophoresis, we demonstrated dose-dependent elevation of 57 kDa cytoskeletal-protein levels for Arecoline. Evidence from immunoblotting assay indicated this 57 kDa cytoskeletal protein was vimentin. The increase in vimentin with Arecoline exposure corresponded to that noted for fibroblasts cultured from OSF patients. Immunohistochemical assay also revealed that vimentin expression was much higher for OSF specimens than for normal buccal mucosa. We suggest these results may advance understanding of the possible pathogenesis for submucous fibrosis through the transformation of normal buccal mucosa as a result of areca quid chewing.

    Free Register to Access Article