Ascorbic acid inhibits replication and infectivity of avian RNA tumor virus.

Ascorbic acid, at nontoxic concentrations, causes a substantial reduction in the ability of avian tumor viruses to replicate in both primary avian tendon cells and chicken embryo fibroblasts. The virus-infected cultures appear to be less transformed in the presence of ascorbic acid by the criteria of morphology, reduced glucose uptake, and increased collagen synthesis. The vitamin does not act by altering the susceptibility of the cells to initial infection and transformation, but instead appears to interfere with the spread of infection through a reduction in virus replication and virus infectivity.

Is the product of the src gene a promoter?

Addition of a potent promoter, 12-O-tetradecanoylphorbol 13-acetate (TPA), to primary avian tendon or chicken embryo fibroblast cells infected with a temperature-sensitive mutant of Rous sarcoma virus produced a complete transformed phenocopy at the nonpermissive temperature by the criteria tested. While normal, uninfected cultures also shifted towards a transformed phenotype after TPA addition, they did not achieve the same degree of morphological and biochemical alteration seen in virus-infected, TPA-treated cells. It is proposed that viral carcinogenesis, despite its rapidity, may occur in two stages: an "initiation" step caused by expression of a part of viral genome other than src (or by integration) and a promotion step (itself a multistep process) caused by the activation of the src gene.

Preferential inhibition of the growth of virus-transformed cells in culture by rifazone-82, a new rifamycin derivative.

Rifazone-8(2), a new rifamycin derivative, is shown to preferentially inhibit the growth of virus-transformed chick cells in culture. Macromolecular synthesis and glucose uptake of transformed cells are also appreciably decreased in the presence of low concentrations of rifazone-8(2) where the normal cells appear unaffected. While rifazone-8(2) is shown to be a selective inhibitor of RNA-directed DNA polymerase in vitro, its action on the growth of transformed cells may involve some other mechanism.

Dynamics of metabolism of normal and virus-transformed chick cells in culture.

Application of steady-state tracer technique to normal and transformed cells in tissue culture allows quantitation of intracellular pool sizes of many metabolites and determination of rate of carbon flow along diverse paths. Using a unique apparatus to control the environmental conditions, we show that the glucose carbon flow into tricarboxylic acid cycle intermediates and amino acids is unchanged upon transformation. The increased glycogen formation and glycolysis varies with the glucose concentration in the medium, correlates with the faster glucose transport of transformed cells, and cannot be explained by a difference in growth rate alone.