PMID: 9440323Jan 24, 1998Paper

Post-exposure processes in Temoporfin-photosensitized cells in vitro: reliance on energy metabolism

Journal of Photochemistry and Photobiology. B, Biology
V KirvelieneB Juodka

Abstract

The progressive responses to photodynamic treatment (lambda > 590 nm) mediated by Temoporfin have been investigated in vitro on two rodent cell lines: BHK and murine hepatoma MH22 cells. Comparisons are made of two light exposure/post-exposure incubation media: Dulbecco's minimal essential medium (DMEM) and phosphate-buffered saline (DPBS) depleted of energy sources. Enhancement of lipid peroxidation is an early response to Temoporfin photosensitization in either experimental set. It is restored to the initial level by subsequent incubation in DMEM, but not in DPBS. The decrease in MTT specific activity and especially lactate dehydrogenase leakage from the cells are faster in DPBS and continue to proceed during the post-exposure incubation in the both media. The intracellular ATP pool is completely depleted within 3 h of post-exposure incubation in DPBS, but not in DMEM where, in contrast, an initial increase in ATP is observed. Based on these preliminary observations, it is presumed that ATP synthesized by injured mitochondria and activated glycolysis is being used to restore the deteriorated cell functions and/or to allow reactions involved in apoptosis to proceed.

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Citations

Jul 7, 1999·Journal of Photochemistry and Photobiology. B, Biology·V O MelnikovaF Guillemin
Aug 29, 2000·Transfusion·Y XiaD J Kuter
Aug 19, 2011·Photochemistry and Photobiology·Mathias O Senge, Johan C Brandt
Aug 22, 2003·Photochemistry and Photobiology·Marie-Hélène TeitenLina Bezdetnaya
Oct 11, 2003·FEBS Letters·Vida KirvelieneBenediktas Juodka
Apr 5, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Ana T P C GomesJosé A S Cavaleiro
Feb 2, 2019·Photodiagnosis and Photodynamic Therapy·G Bœuf-MurailleM Molinari

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis