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- W2941881534 abstract "1745 Introduction: We previously demonstrated that evening primrose extract (EPE) induced apoptosis in Ehrlich ascites tumor cells (EATC), and this effect was specific on tumor cells. We also demonstrated that EPE exposure elicited a rapid increase in intracellular peroxide levels. These changes caused translocation of Bax to mitochondria and a subsequent release of mitochondrial cytochrome c. However, no activation of caspase-3 was observed in EPE-treated EATC. On the other hand, apoptosis-inducing factor (AIF) was translocated from mitohondria to nuclei, which was suppressed with the addition of catalase. Here, we elucidated the intracellular peroxide-dependent mechanism governing cell cycle dynamics during growth arrest by EPE. We also investigated the involvement of polyamines in EPE-induced in increase in apoptosis as well as in EPE-induced decrease in DNA synthesis. Methods: EATC were cultured in Eagle’s MEM containing 10% FCS. 2’,7’-Dichlorodihydrofluorescein diacetate was used as a probe for intracellular ROS formation. The intracellular polyamines were analyzed by HPLC equipped with fluorescence detector. Results: EPE elicited a dose-dependent accumulation of cells in the G1 phase and inhibited DNA synthesis. The cell cycle arrest and inhibition of proliferation in EATC by EPE were associated with decreased Rb phosphorylation. Furthermore, inhibitions of Rb phosphorylation and DNA synthesis by EPE were not suppressed with the addition of catalase. EPE also brought about a significant decrease in intracellular polyamine levels. Furthermore, the addition of polyamines reversed the EPE-induced in cell viavility and suppressed the EPE-induced in intracellular hydrogen peroxide. However the addition of polyamines did not reverse EPE-induced decrease in DNA synthesis and phosphorylation of Rb protein, and EPE-induced translocation of AIF. Conclusion:We demonstrated previously that an EPE-induced rapid increase in intracellular peroxides level triggers off induction of apoptosis in EATC. However the findings in the present study suggest that intracellular peroxides do not cause an EPE-induced G1 arrest. Hence, EPE-induced inhibition of the growth of EATC are via at least two pathways differentially modulated by ROS, notably intracellular peroxides. These are (a) the EPE-induced apoptosis pathway which is dependent on increase in hydrogen peroxide and decrease in polyamines and (b) the EPE-induced of cell proliferation which is hydrogen peroxide independent." @default.
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- W2941881534 date "2005-05-01" @default.
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- W2941881534 title "Evening primrose extract induces apoptosis and inhibits the DNA synthesis in Ehrlich ascites tumor cells via at least two pathways differentially modulated by reactive oxygen species" @default.
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