This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wick, M. M. Articles by Glynn, D. Search for Related Content PubMed PubMed Citation Articles by Wick, M. M. Articles by Glynn, D.

Reduction of Streptozotocin Toxicity by 3-O-Methyl-D-glucose with Enhancement of Antitumor Activity in Murine L1210 Leukemia¹

Division of Clinical Pharmacology and Medical Oncology, Sidney Farber Cancer Institute and Department of Medicine, Peter Bent Brigham Hospital, Harvard Medical School [M. M. W.], and Joslin Research Laboratory, Department of Medicine, Harvard Medical School and Peter Bent Brigham Hospital [A. R., D. G.], Boston, Massachusetts 02115

3-O-Methyl-D-glucose (3-OMG), a nontoxic nonmetabolizable derivative of glucose, is effective in reducing the toxicity of streptozotocin (SZ). In mice the administration of 3-OMG prior to SZ increased the dose that killed 50% of the animals from 240 to 340 mg/kg. Furthermore, the combination of 3-OMG plus nicotinamide (also effective in reducing SZ toxicity) increased the dose that killed 50% of the animals to 540 mg/kg. In L1210 leukemic mice treated with SZ, there was a 2-fold increase in the median survival of animals pretreated with 3-OMG and a 3-fold increase in that of animals pretreated with the combination of 3-OMG and nicotinamide. Neither 3-OMG nor nicotinamide alone enhanced the survival of the leukemic mice. Pretreatment of normal mice with 3-OMG partially prevented the expected fall in hepatic nicotinamide adenine dinucleotide content. This study suggests that 3-OMG, by protecting normal tissue, will permit the administration of larger therapeutic doses of SZ in leukemic L1210 mice. The protective effect of 3-OMG against SZ toxicity appears to be partially mediated through conservation of the nicotinamide adenine dinucleotide content in the tissue.

¹ Supported in part by National Cancer Institute Grant CA 06516 and by American Diabetes Association Grant RR 5673. Part of this work was presented at the Sixty-seventh Annual Meeting of the American Association of Cancer Research, May 4 to 8, 1976, Toronto, Ontario, Canada (18).

² To whom requests for reprints should be addressed, at Sidney Farber Cancer Institute, Boston, Mass. 02115.

Received 4/ 1/77. Accepted 7/26/77.

This article has been cited by other articles:

				P. E. van Eeden, L. B. G. Tee, S. Lukehurst, C.-M. Lai, E. P. Rakoczy, L. D. Beazley, and S. A. Dunlop Early vascular and neuronal changes in a VEGF transgenic mouse model of retinal neovascularization. Invest. Ophthalmol. Vis. Sci., October 1, 2006; 47(10): 4638 - 4645. [Abstract] [Full Text] [PDF]