Elevation of hyperoxia of thymidine kinase activity in hypertrophic V79 lung fibroblasts.
Exposure of V79 cells to hyperoxia (80% O2) for 30 h increased the level of thymidine kinase, a deoxynucleoside salvage enzyme, by approximately 3-fold as compared to cells exposed to room air, but did not cause any significant change in deoxycytidine kinase, the other known deoxynucleoside salvage enzyme. Exposure of cells to anoxia, on the other hand, produced only a slight reduction in thymidine kinase activity. Perturbation in cellular metabolism following exposure to hyperoxia was indicated by marked inhibition of cellular growth and the presence of cellular hypertrophy. Although growth was also inhibited by anoxia, the cell size distribution was minimally altered. The effect of hyperoxia on thymidine kinase suggests that (1) this enzyme may play a role in the modulation of cellular hypertrophy and function following exposure to hyperoxia, and (2) analysis of relative levels of thymidine kinase and deoxycytidine kinase activities may be of value in differentiating between cellular hypertrophy and hyperplasia under some circumstances.
Das
S K
SK
New England Medical Center Hospital, Boston, Mass.
Fanburg
B L
BL
D000818:Animals; D002460:Cell Line; D002852:Chromatography, Ion Exchange; D006224:Cricetinae; D003412:Cricetulus; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects / Q000201:enzymology; D006984:Hypertrophy; D007700:Kinetics; D008168:Lung; D010100:Oxygen / Q000494:pharmacology*; D013937:Thymidine Kinase / Q000302:isolation & purification / Q000378:metabolism*
D013937:Thymidine Kinase; D010100:Oxygen