Potentiation ofTransformation ofRat-Embryo Cells Induced InVitroby3-Methylcholanthrene: Induction ofRat Leukemia VirusgsAntigen inTransformed Cells

Low-passage rat-embryo cells were not transformed by3-methylcholanthrene orby5-bromo-2' deoxyuridine. However, prior treatmentwithbromodeoxy- uridine, followed bytreatmentwithmethylcholanthrene, resulted incelltransformation aboutthreesubpassages afterremovalof the carcinogen. RNA-directed DNA polymerase activity couldnotbedetected ineither normal ortransformed cells. However, gs-1antigen specific for ratC-typeRNA viruswas detected incultures derived frombromodeoxyuridine-treated cells. No gs-1antigen fortheC-type RNA viruswasdetected incultures thathad notbeentreated withbromodeoxyuridine duringthe25 subpassages oftheseexperiments. High-passage rat-embryo cells, derived fromadifferent cellpool, weretransformed byeither methylcholanthrene ordimethylbenzanthracene withoutpriorinfection with an exogenous virus, and withoutpriortreatmentwith bromodeoxyuridine. gs-1antigen forC-type RNA virus was alsodetected in4of4randomlyselected transformed cell lines; thegs-1antigen wasnotdetected inanyof4non- transformed control cultures. Considering theseandpre- viously published findings, we concludethatthelow- passagecellscannotbe transformed by methylcholan- threnebecause ofpowerful cellular controls overtheendo- genousvirus. Bromodeoxyuridine triggers someexpres- sionsoftheendogenous virus; thus,thebromodeoxy- uridine-treated cells aremoresusceptible tothetrans- forming effects ofmethylcholanthrene. High-passage rat cells donotmaintainperfect control overexpression of theirendogenous virus; thecellcultures aresusceptible tothetransforming effects ofchemical carcinogens. Inprevious publications, itwasshownthatcertain low- passage rat(1-3) andmouse(4)embryo-cell cultures were refractory tothetransforming effects ofdiethylnitrosamine, 3 methylcholanthrene,