ArticleArchives of drug information2009
Ascorbic Acid Potentiation of Arsenic Trioxide Anticancer Activity Against Acute Promyelocytic Leukemia.
Article in Archives of drug information, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 28 citations in OpenAlex.
- Ascorbic acid potentiates the Giardia duodenalis growth inhibitory activity of pure Terminalia ferdinandiana Exell compounds.Parasitology research · 2020Article
- Article
- Biochemical changes associated with ascorbic acid-cisplatin combination therapeutic efficacy and protective effect on cisplatin-induced toxicity in tumor-bearing mice.Toxicology reports · 2015Article
- Dual effect of oxidative stress on leukemia cancer induction and treatment.Journal of experimental & clinical cancer research : CR · 2014Review
- Vitamin D3 potentiates the antitumorigenic effects of arsenic trioxide in human leukemia (HL-60) cells.Experimental hematology & oncology · 2014Article
- In vitro assessment of oxidative stress and apoptotic mechanisms of garlic extract in the treatment of acute promyelocytic leukemia.Journal of cancer science & therapy · 2012Article
- Candidate single nucleotide polymorphism markers for arsenic responsiveness of protein targets.Bioinformatics and biology insights · 2010Article
- Basic mechanisms of arsenic trioxide (ATO)-induced apoptosis in human leukemia (HL-60) cells.Journal of hematology & oncology · 2010Article
- Heavy metal toxicity and the environment.Experientia supplementum (2012)Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
introductionAcute promyelocytic leukemia (APL) is a malignant disorder of the white blood cells. Arsenic trioxide (As(2)O(3)) has been used as a therapeutic agent to treat APL and other tumors. Studies suggest that ascorbic acid (AA) supplementation may improve the clinical outcome of As(2)O(3) for APL patients. Our aim was to use human leukemia (HL-60) APL-cells as an in vitro test model to evaluate the effect of physiologic doses of AA on As(2)O(3)-induced toxicity and apoptosis of HL-60 cells.
methodsHL-60 cells were treated either with a pharmacologic dose of As(2)O(3) alone and with several physiologic doses of AA. Cell survival was determined by trypan blue exclusion test. The extent of oxidative cell/tissue damage was determined by measuring lipid hydroperoxide concentration by spectrophotometry. Cell apoptosis was measured by flow cytometry using Annexin-V and propidium iodide (PI) staining.
resultsAA treatment potentiates the cytotoxicity of As(2)O(3) in HL-60 cells. Viability decreased from (58 +/- 3)% in cells with As(2)O(3) alone to (47 +/- 2)% in cells treated with 100 microM AA and 6 microg/mL As(2)O(3) with P < 0.05. There was a significant (P < 0.05) increase in lipid hydroperoxide concentrations in HL-60 cells co-treated with AA compared to As(2)O(3) alone. Flow cytometry assessment (Annexin V FITC/PI) suggested that AA co-treatment induces more apoptosis of HL-60 cells than did As(2)O(3) alone, but this was not statistically significant. Taken together, our experiment indicates that As(2)O(3) induced in vitro cell death and apoptosis of HL-60 cells. Administration of physiologic doses of AA enhanced As(2)O(3)-induced cytotoxicity, oxidative cell/tissue damage, and apoptosis of HL-60 cells through externalization of phosphatidylserine.
conclusionsThese suggest that AA may enhance the cytotoxicity of As(2)O(3), suggesting a possible future role of AA/As(2)O(3) combination therapy in patients with APL.
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Registered trials
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