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Ascorbic acid alleviates toxicity of paclitaxel without interfering with the anticancer efficacy in mice.
MedLine Citation:
PMID:  23176798     Owner:  NLM     Status:  In-Data-Review    
Paclitaxel is used extensively as a chemotherapeutic agent against a broad range of tumors but often leads to the early termination of treatment due to severe toxic side effects. In this study, we hypothesized that ascorbic acid could reduce the toxic side effects without interfering with the anticancer effect of paclitaxel. To demonstrate this, we examined the effect of the combinational treatment of ascorbic acid and paclitaxel using H1299 (a non-small cell lung cancer cell line) and BALB/c mice implanted with or without sarcoma 180 cancer cells. In H1299 cells, the anticancer effects of the combinational treatment with paclitaxel and ascorbic acid were up to 1.7-foldhigher than those of single-agent paclitaxel treatment. In addition, it was shown that the viability of the HEL299 normal cells was up to 1.6-fold higher with the combinational treatment than with paclitaxel treatment alone. In vivo mouse experiments also showed that mice co-treated with paclitaxel and ascorbic acid did not exhibit the typical side effects induced by paclitaxel, such as a reduction in the numbers of white blood cells and red blood cells and the level of hemoglobin (P < .05). The analysis of cancer-related gene expression by quantitative real-time polymerase chain reaction and immunohistochemistry revealed that the combinational treatment suppressed cancer cell multiplication. Taken together, these results suggest that combinational chemotherapy with ascorbic acid and paclitaxel not only does not block the anticancer effects of paclitaxel but also alleviates the cytotoxicity of paclitaxel in vivo and in vitro.
Jin-Hee Park; Keith R Davis; Gunsup Lee; Manyong Jung; Yuchul Jung; Jungan Park; Sang-Yeop Yi; Myung-Ah Lee; Sukchan Lee; Chang-Hwan Yeom; Jin Kim
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Publication Detail:
Type:  Journal Article     Date:  2012-10-26
Journal Detail:
Title:  Nutrition research (New York, N.Y.)     Volume:  32     ISSN:  1879-0739     ISO Abbreviation:  Nutr Res     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-11-26     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8303331     Medline TA:  Nutr Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  873-83     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
Department of Biomedical Science, College of Medicine, The Catholic University of Korea, Seoul, 137-701, South Korea; Department of Anatomy and Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Seoul, 137-701, South Korea.
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