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PHTHALOCYANINE PHOTOSENSITIZATION OF MAMMALIAN CELLS: BIOCHEMICAL and ULTRASTRUCTURAL EFFECTS
Year:
1987
Source of publication :
Photochemistry and Photobiology
Authors :
Rosenthal, Ionel
;
.
Volume :
46
Co-Authors:
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
Facilitators :
From page:
651
To page:
656
(
Total pages:
6
)
Abstract:
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
Note:
Related Files :
Animal
biosynthesis
light
metabolism
nucleic acid
Nucleic acids
Organometallic Compounds
proteins
Show More
Related Content
More details
DOI :
10.1111/j.1751-1097.1987.tb04827.x
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
28243
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:37
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Scientific Publication
PHTHALOCYANINE PHOTOSENSITIZATION OF MAMMALIAN CELLS: BIOCHEMICAL and ULTRASTRUCTURAL EFFECTS
46
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
PHTHALOCYANINE PHOTOSENSITIZATION OF MAMMALIAN CELLS: BIOCHEMICAL and ULTRASTRUCTURAL EFFECTS
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
Scientific Publication
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