Sodium ascorbate potentiates the growth inhibitory effect of certain agents on neuroblastoma cells in culture.

Abstract

Mouse neuroblastoma (NB) [NBP2] cells in culture were more sensitive to sodium L-ascorbate than were rat glioma [C-6] cells by the criterion of growth inhibition (due to cell death and reduction in cell division). Sodium L-ascorbate at nonlethal concentrations potentiated the effect of 5-fluorouracil (FUra), X-irradiation, bleomycin, RO20-1724 [4-[(3-butoxy-4-methoxyphenyl)methyl]-2-imidazolidinone], prostaglandin E1 and sodium butyrate on NB cells but did not produce such as effect on glioma cells. Sodium L-ascorbate did not enhance the effect of vincristine, 6-thioguanine or 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU) except at higher drug doses and it reduced the cytotoxic effect of methotrexate and 5-(3,3-dimethyl-1-triazeno)-imidazole-4-carboxamide (DTIC) on NB cells. Sodium D-ascorbate produced effects similar to those produced by sodium L-ascorbate on NB cells. L-Ascorbic acid-2-sulfate (Ba salt) affected neither the growth rat nor the effect of 5-FUra on NB cells. Glutathione, a reducing agent, was more toxic to NB cells in comparison to D- or L-ascorbate; however, at a similar concentration it failed to potentiate the effect of 5-FUra on NB cells.