Ascorbate stabilizes the differentiated state and reduces the ability of Rous sarcoma virus to replicate and to uniformly transform cell cultures.
In primary avian tendon cells, Rous sarcoma virus can coexist or completely take over the cell. Infection, at high multiplicity or under conditions that promote high virus production (no ascorbate and high serum concentrations), results in almost complete oncogenic transformation of the culture. This is indicated in part by a radical change in morphology, growth at high cell density, and a dramatic drop in the production of procollagen from approximately 50% to approximately 3% of total protein synthesis. In contrast, infection at low multiplicity, infection with a replication defective virus, or the presence of ascorbate restrict the ability of the virus to transform the culture. Thus, there appears to be a balance between the normal and transformed states of the cell that can be shifted depending on the cellular environment and the level of infection. Ascorbate stabilizes the normal state by reducing virus production and promoting the synthesis of differentiated proteins.
Schwarz
R I
RI
Cell and Molecular Biology Division, Lawrence Berkeley Laboratory, University of California, Berkeley 94720.
D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology*; D001358:Avian Sarcoma Viruses / Q000187:drug effects* / Q000502:physiology; D001769:Blood; D002454:Cell Differentiation / Q000187:drug effects; D002471:Cell Transformation, Neoplastic / Q000187:drug effects; D002478:Cells, Cultured; D003470:Culture Media; D001357:Sarcoma, Avian / Q000473:pathology; D013710:Tendons / Q000196:embryology / Q000473:pathology; D014779:Virus Replication / Q000187:drug effects*
D003470:Culture Media; D001205:Ascorbic Acid