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Photosensitization Reaction‐Induced Acute Electrophysiological Cell Response of Rat Myocardial Cells in Short Loading Periods of Talaporfin Sodium or Porfimer Sodium
Author(s) -
Ito Arisa,
Kimura Takehiro,
Miyoshi Shunichiro,
Ogawa Satoshi,
Arai Tsunenori
Publication year - 2010
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.1751-1097.2010.00846.x
Subject(s) - photosensitizer , chemistry , biophysics , electrophysiology , sodium , fluorescence , intracellular , confocal , fluorescence microscope , membrane potential , sodium channel , cell , irradiation , confocal microscopy , photochemistry , biochemistry , medicine , microbiology and biotechnology , biology , optics , physics , organic chemistry , nuclear physics
Electrophysiological responses of rat myocardial cells to exogenous photosensitization reactions for a short period of incubation with two photosensitizers, talaporfin sodium or porfimer sodium, were measured in a subsecond time scale. The loading period of the photosensitizer when the photosensitizer might not be taken up by the cells was selected as 15 min, which was determined by the fluorescence microscopic observation. We measured the intracellular Ca 2+ concentration ([Ca 2+ ] in ) by using a fluorescent Ca 2+ indicator, Fluo‐4 AM, under a high‐speed confocal laser microscope to evaluate the acute electrophysiological cell response to the photosensitization reaction. The measured temporal change in Fluo‐4 fluorescence intensity indicated that the response to the photosensitization reaction might be divided into two phases in both photosensitizers. The first phase is acute response: disappearance of Ca 2+ oscillation when irradiation starts, which might be caused by ion channel dysfunction. The second phase is slow response: [Ca 2+ ] in elevation indicating influx of Ca 2+ due to the concentration gradient. The continuous Ca 2+ influx followed by changes in cell morphology suggested micropore formation on the surface of the cell membrane, resulting in necrotic cell death.