12 J / cm 2 x 5 min + 200u / mL catalase. No change Protected before irradiation
DISCUSSION
● The toxic effect of visible light or H 2 O 2 is dose dependent cardiomyocytes
● Illumination below 3.6J / cm 2 or concentrations below 24 µ M H 2 O 2 cause no harm to most of the cells 24 hours after treatment. Therefore, visible light illumination with energy less than 3.6J / cm 2 appears safe for cardiomyocytes.
● The results suggest that the kinetics of [ Ca 2 + ] may reflect the ability of cells to adapt to changes due to H 2 O 2 and light. However, the light treatment of 3.6J / cm 2 and a H 2 O 2 concentrations( 12uM) are tolerated dose Cell.
● Linear kinetics, observed after 12J / cm 2 LEVL illumination change in the presence of catalase also prevented cell damage. Suggest that the kinetics of [ Ca 2 + ] may reflect the ability of cells to adapt to the changes caused by H 2 O 2 and light. However, treatment with light of 3.6J / cm2 and a low concentration of H 2 O 2( 12 µ M) are tolerated dose Cell.
● The kinetics of the increase in [ Ca 2 + ] has been studied to reflect an adaptive response of the cells to oxidative stress.
● The elevation of [ Ca 2 + ] can not be attributed to ROS damage on lipid peroxidation of the membrane or membrane permeabilization to the influx of Ca 2 +, as suggested earlier in photodynamic systems.
● The change in [ Ca 2 + ] and therefore the elevation of ROS in undamaged cells is partly explained by the ability of ROS to mediate direct phosphorylation or indirectly transporters calcium or the ability of ROS to oxidize thiol groups to disulfides in calcium transporters. Calcium conveyors in muscle cells are known to be very sensitive to oxidation. Thiol oxidation by ROS can cause a structural change in the conveyors, which may inhibit or enhance their function. In the present study, we found that the increase of [ Ca 2 + ] after illumination by LEVL or application of H 2 O 2 18 µ M inhibitor is reduced by the calcium channel voltage-dependent, verapamil.
● The calcium channel voltage-dependent L-type myocytes suggests having a redox-sensitive receptor that can be activated by ROS.
● The increase in [ Ca 2 + ] L-type channels may even cause a further increase in [ Ca 2 + ] by inducing Ca 2 + release from the sarcoplasmic reticulum. Such a movement mechanism is known as a mechanism of calcium-induced calcium release.
● The kinetics of [ Ca 2 + ] may indicate the future of the cells 24 h after treatment. The rapid increase in [ Ca 2 + ] was correlated with irreversible damage to the cell while the transient increase correlated with undamaged cells. Has shown that a prolonged rise in [ Ca 2 + ] can be lethal, whereas cells can prevent death signals using low [ Ca 2 + ].