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Calcium as a Modulator of Photosensitized Killing of H9c2 Cardiac Cells ¶
Author(s) -
Valenzeno Dennis Paul,
Tarr Merrill
Publication year - 2001
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 - 10.1562/0031-8655(2001)0740605caamop2.0.co2
Subject(s) - trypan blue , biophysics , rose bengal , tetraethylammonium , chemistry , tetrodotoxin , potassium channel , calcium , membrane potential , potassium channel blocker , intracellular , reversal potential , cell , patch clamp , biochemistry , potassium , biology , receptor , organic chemistry
Illumination of H9c2 rat heart cells in the presence of Rose Bengal resulted in dose‐dependent cell killing (assessed by trypan blue staining) and modification of ionic currents flowing through the heart cell membrane. Inhibitors of voltage‐gated ionic currents were shown to have little effect on cell killing. Ionic current measurements were used to assess the increase in leak conductance of these cells, which has been suggested to be a causal factor in killing of other cell types (1). Inhibitors of voltage‐gated ionic currents, including the sodium channel blocker tetrodotoxin (100 μ M ) and the calcium channel blocker lanthanum (10 μ M ) were shown to have little effect on cell killing. The potassium channel inhibitor tetraethylammonium (20 m M ) inhibited cell killing, but the effect is viewed as being caused by an inhibition of leak current. The time course of block of voltage‐activated ionic currents during illumination, in the presence of Rose Bengal, was rapid compared with that for induction of leak current and for cell killing. These observations are consistent with a role for leak current in photosensitized killing of cardiac cells. They are interpreted with respect to calcium influx through the leak current pathway as a trigger for the cellular response.