Premium
PHTHALOCYANINE PHOTOSENSITIZATION OF MAMMALIAN CELLS: BIOCHEMICAL and ULTRASTRUCTURAL EFFECTS
Author(s) -
BenHur E.,
Green M.,
Prager A.,
Kol R.,
Rosenthal I.
Publication year - 1987
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1987.tb04827.x
Subject(s) - rna , uridine , metabolism , dna , protein biosynthesis , biochemistry , thymidine , growth inhibition , chinese hamster , microbiology and biotechnology , biology , chemistry , mitochondrion , cell culture , cell growth , genetics , gene
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.