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Pharmacologic ascorbic acid concentrations selectively kill cancer cells: action

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Pharmacologic ascorbic acid concentrations selectively kill cancer cells:

action as a pro-drug to deliver hydrogen peroxide to tissues.

_http://www.ncbi.nlm.nih.gov/pubmed/16157892_

(http://www.ncbi.nlm.nih.gov/pubmed/16157892)

 

_Chen Q_ (http://www.ncbi.nlm.nih.gov/pubmed?term= " Chen%20Q " [Author]) ,

_Espey MG_ (http://www.ncbi.nlm.nih.gov/pubmed?term= " Espey%20MG " [Author]) ,

_Krishna MC_ (http://www.ncbi.nlm.nih.gov/pubmed?term= " Krishna%20MC " [Author]) ,

_Mitchell JB_

(http://www.ncbi.nlm.nih.gov/pubmed?term= " Mitchell%20JB " [Author]) , _Corpe CP_

(http://www.ncbi.nlm.nih.gov/pubmed?term= " Corpe%20CP " [Author]) , _Buettner GR_

(http://www.ncbi.nlm.nih.gov/pubmed?term= " Buettner%20GR " [Author]) , _Shacter E_

(http://www.ncbi.nlm.nih.gov/pubmed?term= " Shacter%20E " [Author]) , _Levine M_

(http://www.ncbi.nlm.nih.gov/pubmed?term= " Levine%20M " [Author]) .

 

 

Molecular and Clinical Nutrition Section, National Institute of Diabetes

and Digestive and Kidney Diseases, National Institutes of Health, Bethesda,

MD 20892, USA.

 

 

Human pharmacokinetics data indicate that i.v. ascorbic acid (ascorbate)

in pharmacologic concentrations could have an unanticipated role in cancer

treatment. Our goals here were to test whether ascorbate killed cancer cells

selectively, and if so, to determine mechanisms, using clinically relevant

conditions. Cell death in 10 cancer and 4 normal cell types was measured

by using 1-h exposures. Normal cells were unaffected by 20 mM ascorbate,

whereas 5 cancer lines had EC(50) values of <4 mM, a concentration easily

achievable i.v. Human lymphoma cells were studied in detail because of their

sensitivity to ascorbate (EC(50) of 0.5 mM) and suitability for addressing

mechanisms. Extracellular but not intracellular ascorbate mediated cell death,

which occurred by apoptosis and pyknosis/necrosis. Cell death was

independent of metal chelators and absolutely dependent on H(2)O(2) formation.

Cell

death from H(2)O(2) added to cells was identical to that found when

H(2)O(2) was generated by ascorbate treatment. H(2)O(2) generation was

dependent

on ascorbate concentration, incubation time, and the presence of 0.5-10%

serum, and displayed a linear relationship with ascorbate radical formation.

Although ascorbate addition to medium generated H(2)O(2), ascorbate

addition to blood generated no detectable H(2)O(2) and only trace detectable

ascorbate radical. Taken together, these data indicate that ascorbate at

concentrations achieved only by i.v. administration may be a pro-drug for

formation of H(2)O(2), and that blood can be a delivery system of the pro-drug

to

tissues. These findings give plausibility to i.v. ascorbic acid in cancer

treatment, and have unexpected implications for treatment of infections where

H(2)O(2) may be beneficial.

 

 

PMID: 16157892 [PubMed - indexed for MEDLINE]

 

PMCID: PMC1224653

 

 

 

 

 

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