Mitogenic inhibition and effect on survival of mice bearing L1210 leukemia using a combination of dehydroascorbic acid and hydroxycobalamin

Me, Poydock; Harguindey, Salvador; T, Hart; Takita, Hiroshi; Kelly, Daniel

doi:10.1097/00000421-198506000-00013

Cited by 16 publications

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“…When ascites tumors were exposed to a mixture of vitamins B)2 and C, cell mitotic activities were inhibited [13,16]. It is believed that the duration of cell cycle is regulated by the duration of the G1 period.…”

Section: Resultsmentioning

confidence: 99%

“…In vitro studies indicated that vitamins B12 and C were toxic to mouse LI210 leukemia cells, but nonneoplastic L929 cells were not affected [16]. The survival rate of the tumor-bearing animals was increased after the treatment with vitamins B12 and C, and no apparent toxic side effect on the host was observed [14,16]. However, results of an experiment with Fisher CDF rats indicated that a mixture of vitamins B12 and C had no effect on the growth of L9 gliosarcoma in rats and that no difference in survival time between treatment group and control group was observed [ 17].…”

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confidence: 99%

“…This mixture of vitamins also inhibited the growth of several mouse ascites and solid tumors, including P388 leuke mia, Krebs 2, and Ehrlich carcinoma [14,15]. In vitro studies indicated that vitamins B12 and C were toxic to mouse LI210 leukemia cells, but nonneoplastic L929 cells were not affected [16]. The survival rate of the tumor-bearing animals was increased after the treatment with vitamins B12 and C, and no apparent toxic side effect on the host was observed [14,16].…”

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confidence: 99%

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Cytotoxic Activity of Cobalamin in Cultured Malignant and Nonmalignant Cells

1990

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The cytotoxic effect of cobalamin (vitamin B₁₂) on the growth of malignant and nonmalignant cell lines in culture has been examined. Among the four cobalamins studied, 5’-deoxyadenosylcobalamin, an enzymatically active derivative, was an effective cytotoxic agent. The data indicated that adenosylcobalamin seemed to act selectively on fast-growing malignant cells. Methylcobalamin was also effective at elevated concentrations. Cyanocobalamin was not toxic to all cell lines studied. Hydroxocobalamin at very high concentrations was able to slightly decrease growth of certain cell lines. The results support the hypothesis that the cytotoxic effect of cobalamin was associated with the metabolic activities of this vitamin at the cellular level. Also, cobalamin may be a potential antitumor agent.

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Section: Resultsmentioning

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Cytotoxic Activity of Cobalamin in Cultured Malignant and Nonmalignant Cells

1990

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“…Thus, it is highly likely that irreversible modifications of crucial cysteine residues inhibit enzymatic activity, modify function and structure of important cellular proteins possibly leading to destabilized cellular homeostasis. In this regard, protein S‐ascorbylation could explain in part the observed toxicity of DHA on certain tumors in vitro and in vivo . DHA is easily taken up by cells through glucose transporters 1 and 4 .…”

Section: Discussionmentioning

confidence: 99%

Characterization of dehydroascorbate‐mediated modification of glutaredoxin by mass spectrometry

et al. 2015

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Ascorbate is as a potent antioxidant in vivo protecting the organism against oxidative stress. In this process, ascorbate is oxidized in two steps to dehydroascorbate (DHA), which if not efficiently reduced back to ascorbate decomposes irreversibly to a complex mixture of products. We demonstrate that a component of this mixture specifically reacts with the thiol group of cysteine residues at physiological pH to give a protein adduct involving the addition of a 5-carbon fragment of DHA (+112 Da). Incubations of glutaredoxin-1 expressed in Escherichia coli and dehydroascorbate revealed abundant adducts of +112, +224 and +336 Da due to the addition of one, two and three conjugation products of DHA, respectively. ESI-MS of carbamidomethylated glutaredoxin-1 before incubation with DHA, deuterium exchange together with tandem mass spectrometry analysis and LC-ESIMS/MS of modified peptides confirmed structure and sites of modification in the protein. Modification of protein thiols by a DHA-derived product can be involved in oxidative stress-mediated cellular toxicity.

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“…Mice treated with vitamin B]2 survived longer than did untreated controls. Vitamin B12 also inhibited the growth of liver tumors induced by /;-dimelhy!aminoazo benzene in rats [14], A mixture of vitamin B12 and vita min C was able to inhibit the growth of certain mouse ascites or solid tumors and to increase the survival rate of tumor bearing mice [15][16][17], However, in another study with Fischer CDF rats, a mixture of vitamins B12 and C had no effects on the growth of L9 gliosarcoma, and no differences in survival time between treatment and con trol group were observed [18]. Furthermore, in some cases, vitamin B|2 enhanced the growth of fibrosarcoma in rats and of Rous sarcoma in chickens [ 19].…”

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Influence of Cobalamin on the Survival of Mice Bearing Ascites Tumor

Tsao

Myashita²

1993

Pathobiology

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The effect of cobalamin (vitamin B₁₂) on the survival time of mice bearing P388 leukemia has been examined. Among the three cobalamins studied, the enzymatically active derivatives, methylcobalamin and 5’-deoxyadenosylcobalamin, were able to significantly increase the survival time of mice implanted intraperitoneally with the tumor cells. The pharmaceutical form, cyanocobalamin, was not active. The antitumor activity of these cobalamins may be associated with their functions in metabolism.

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Mitogenic inhibition and effect on survival of mice bearing L1210 leukemia using a combination of dehydroascorbic acid and hydroxycobalamin

Cited by 16 publications

References 0 publications

Cytotoxic Activity of Cobalamin in Cultured Malignant and Nonmalignant Cells

Cytotoxic Activity of Cobalamin in Cultured Malignant and Nonmalignant Cells

Characterization of dehydroascorbate‐mediated modification of glutaredoxin by mass spectrometry

Influence of Cobalamin on the Survival of Mice Bearing Ascites Tumor

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