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Ascorbic Acid Synergistically Potentiates Phloxine B‐induced Photocytotoxicity in Human Acute Promyelocytic Leukemia Cells
Author(s) -
Qi Hang,
Wu Qian,
Abe Naomi,
Saiki Shunya,
Zhu Beiwei,
Murata Yoshiyuki,
Nakamura Yoshimasa
Publication year - 2014
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21549
Subject(s) - acute promyelocytic leukemia , chemistry , ascorbic acid , glutathione , p38 mitogen activated protein kinases , mapk/erk pathway , kinase , antioxidant , pharmacology , oxidative stress , biochemistry , catalase , protein kinase a , enzyme , biology , food science , retinoic acid , gene
Ascorbic acid (AsA) is known as an antioxidant but concomitantly possesses a pro‐oxidant property. Because the impact of AsA on photodynamic therapy response is unclear, we investigated the effect of AsA on photocytotoxicity induced by phloxine B in human acute promyelocytic leukemia HL‐60 cells. AsA synergistically enhanced phloxine B‐induced photocytotoxic effects, including inhibition of cell proliferation, DNA ladder formation, and caspase‐3 activation, whereas AsA itself showed no photocytotoxicity. AsA also enhanced the consumption of the reduced glutathione level compared with the cells treated with phloxine B alone under the light condition. Combination of AsA with phloxine B under the light condition enhanced the phosphorylation of c‐Jun N‐terminal kinase and p38 mitogen‐activated protein kinase (MAPK). These effects were completely cancelled by catalase. These results suggest that AsA synergistically enhances phloxine B‐induced photocytotoxicity, possibly through the extracellular oxidative stress‐dependent MAPK pathway activation.