Ben‐Hur, E., Nuclear Research Center-Negev, P.O. Box 9001, Beer-Sheva, 84190, Israel
Green, M., Nuclear Research Center-Negev, P.O. Box 9001, Beer-Sheva, 84190, Israel
Prager, A., Nuclear Research Center-Negev, P.O. Box 9001, Beer-Sheva, 84190, Israel
Kol, R., Nuclear Research Center-Negev, P.O. Box 9001, Beer-Sheva, 84190, Israel
Rosenthal, I., Volcani Center, P.O. Box 6, Bet-Dagan, Israel

Abstract The incorporation of thymidine, uridine and leucine into DNA, RNA and proteins, respectively, was measured in log‐phase Chinese hamster cells photosensitized by chloroaluminum phthalo‐cyanine tetrasulfonate (A1PCS). Post‐treatment synthesis of all macromolecules was inhibited. The inhibition became progressively more pronounced with time, reaching a maximum at ca. 3 h after treatment. The differences between relative sensitivity of protein, RNA and DNA syntheses to A1PCS photosensitization, were not statistically significant. Some of the observed inhibition was due to a reduced uptake of the labeled precursors from the growth medium. Energy metabolism, as reflected by glucose oxidation, was sensitive to A1PCS plus light. Inhibition of glucose oxidation was evident immediately after treatment, and became more pronounced with time. Following a sublethal light fluence, maximum inhibition was observed at 3 h and there was a gradual recovery at later times. Inhibition of glucose oxidation was about two fold higher in plateau‐phase compared to log‐phase cells. The former were also twice as sensitive with respect to cell killing. These results suggest that inhibition of glucose oxidation induced by mitochondrial damage as seen in human lymphocytes, may be a primary cause for AlPCS‐photosensitized cell killing. Copyright © 1987, Wiley Blackwell. All rights reserved