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    Effects of Isothiocyanates on Antioxidant Response Element - mediated Gene Expression and Apoptosis = Effects of Isothiocyanates on Antioxidant Response Element - mediated Gene Expression and Apoptosis

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    https://www.riss.kr/link?id=A76061286

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    The pro-apoptotic effect of phenethyl isothiocyanate (PEITC) and the role of glutathione (GSH) in sulforaphane (SFN)-induced antioxidant response element-dependent gene expression were investigated. The caspase-3 and caspase-9 activities were stimulated by PEITC. The release of cytochrome c was time- and dose- dependent. SP600125 suppressed apoptosis induced by PEITC. Similarly, this JNK inhibitor attenuated both cytochrome c release and caspase-3 activation induced by PEITC. SFN is converted to the glutathione conjugate by glutathione S-transferases (GSTs). It was accumulated in mammalian cells by up to several hundred-fold over the extracellular concentration, by conjugation with intracellular GSH. The induction of ARE by SFN was 8.6-fold higher than by SFN-NAC. The decrease in ARE expression at higher concentrations of SFN and SFN-NAC was correlated with the accelerated apoptotic cell death, with a dosedependent activation of caspase 3 activity by SFN. Upon addition of extracellular GSH within 6 hr of treatment with SFN, the effect on ARE expression was blocked almost completely.
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    The pro-apoptotic effect of phenethyl isothiocyanate (PEITC) and the role of glutathione (GSH) in sulforaphane (SFN)-induced antioxidant response element-dependent gene expression were investigated. The caspase-3 and caspase-9 activities were stimulat...

    The pro-apoptotic effect of phenethyl isothiocyanate (PEITC) and the role of glutathione (GSH) in sulforaphane (SFN)-induced antioxidant response element-dependent gene expression were investigated. The caspase-3 and caspase-9 activities were stimulated by PEITC. The release of cytochrome c was time- and dose- dependent. SP600125 suppressed apoptosis induced by PEITC. Similarly, this JNK inhibitor attenuated both cytochrome c release and caspase-3 activation induced by PEITC. SFN is converted to the glutathione conjugate by glutathione S-transferases (GSTs). It was accumulated in mammalian cells by up to several hundred-fold over the extracellular concentration, by conjugation with intracellular GSH. The induction of ARE by SFN was 8.6-fold higher than by SFN-NAC. The decrease in ARE expression at higher concentrations of SFN and SFN-NAC was correlated with the accelerated apoptotic cell death, with a dosedependent activation of caspase 3 activity by SFN. Upon addition of extracellular GSH within 6 hr of treatment with SFN, the effect on ARE expression was blocked almost completely.

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    목차 (Table of Contents)

    • ABSTRACT
    • INTRODUCTION
    • MATERIALS AND METHODS
    • RESULTS AND DISCUSSION
    • ACKNOWLEDGEMENTS
    • ABSTRACT
    • INTRODUCTION
    • MATERIALS AND METHODS
    • RESULTS AND DISCUSSION
    • ACKNOWLEDGEMENTS
    • REFERENCES
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