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• W2365641305 endingPage "109" @default.
• W2365641305 startingPage "102" @default.
• W2365641305 abstract "Recently, arsenic trioxide (As₂O₃) was reported to induce clinical remission in patients with acute promyelocytic leukemia. Modulation of protein phosphorylation by binding to the vicinal thiols has been suggested as a possible mechanism. We found that phenylarsine oxide, a strong vicinal thiol-binding agent, neither induced nuclear fragmentation or DNA laddering nor increased caspase activity in NB4 cells; however, As₂O₃ and a weak thiol-binding agent, dimethylarsinic acid, did increase activity. Dithiothreitol (DTT) effectively suppressed the phenylarsine oxide-inhibited cellular reductive capacity, but unexpectedly, enhanced As₂O₃-induced apoptosis in NB4 cells. As₂O₃-induced and As₂O₃-plus-DTT-induced apoptosis in NB4 cells was modulated by oxidant modifiers, but not by nitric oxide synthase inhibitors. These results demonstrate that DTT, a dithiol agent and known antidote for trivalent inorganic arsenic, enhances the toxicity of As₂O₃, thereby opening a new research direction for the mechanisms of arsenic toxicity and perhaps also helping in the development of new therapeutic strategies for treating leukemias." @default.
• W2365641305 created "2016-06-24" @default.
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• W2365641305 date "1999-07-01" @default.
• W2365641305 modified "2023-10-15" @default.
• W2365641305 title "Dithiothreitol Enhances Arsenic Trioxide-Induced Apoptosis in NB4 Cells" @default.
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• W2365641305 doi "https://doi.org/10.1124/mol.56.1.102" @default.
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