The reversal of effects of methotrexate on toxicity and glucose transport reduction by thymidine in Ehrlich ascites tumor bearing mice.
Methotrexate (MTX) suppressed the growth of Ehrlich ascites tumor cells in vivo and reduced the cellular uptake of glucose and the density of glucose transporters on the tumor cell surface. MTX inhibition of tumor growth was partially prevented by concurrent administration of thymidine. At the same time, the rate of cellular glucose uptake, the density of glucose transporters on the cell as well as the extent of thymidine, uridine and leucine incorporation were significantly increased.
D000818:Animals; D001665:Binding Sites / Q000187:drug effects; D001693:Biological Transport, Active / Q000187:drug effects; D002286:Carcinoma, Ehrlich Tumor / Q000378:metabolism / Q000473:pathology*; D002455:Cell Division / Q000187:drug effects; D002462:Cell Membrane / Q000378:metabolism; D003571:Cytochalasin B / Q000378:metabolism; D003837:Deoxy Sugars / Q000378:metabolism*; D003847:Deoxyglucose / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology; D008727:Methotrexate / Q000633:toxicity*; D051379:Mice; D008813:Mice, Inbred ICR; D013936:Thymidine / Q000494:pharmacology*
D003837:Deoxy Sugars; D003571:Cytochalasin B; D003847:Deoxyglucose; D005947:Glucose; D013936:Thymidine; D008727:Methotrexate