Hubmer A, Hermann A, Uberriegler K, Krammer B
Institute of Physics and Biophysics, University of Salzburg, Austria.
Photochem Photobiol. 1996 Jul;64(1):211-5. doi: 10.1111/j.1751-1097.1996.tb02444.x.
Photodynamically induced changes in the cytoplasmic free calcium concentration ([Ca2+]i) and its role in cell damage were investigated in human skin fibroblasts using confocal laser microscopy. Fluorescence and absorbance spectrophotometry measurements indicate that the photosensitizer aluminum phthalocyanine tetrasulfonate (AIPcS4) binds to the plasma membrane and only after irradiation is able to enter the cells, causing massive morphologic alterations. Upon irradiation of sensitizer-treated cells, the increase in [Ca2+]i is related to the amount of light and extracellular [Ca2+]e. The increase in [Ca2+]i was substantially reduced in the absence of [Ca2+]a. Cell damage or death after photodynamic treatment was prevented and shifted toward higher fluence by increasing [Ca2+]i at high [Ca2+]e and was greater at low [Ca2+]e. Application of Ca2+ channel blockers, such as Co2+, Cd2+ or verapamil, could not prevent the increase of [Ca2+]i. Our results indicate that activation of the photosensitizer, AIPcS4, causes an influx of Ca2+, which protects cells from, photodamage. At low [Ca2+]e and high fluence values, release of Ca2+ from internal stores probably as a protective measure occurs in order to increase the [Ca2+]i.
利用共聚焦激光显微镜研究了光动力诱导的人皮肤成纤维细胞胞质游离钙浓度（[Ca2+]i）变化及其在细胞损伤中的作用。荧光和吸光度分光光度法测量表明，光敏剂四磺基铝酞菁（AIPcS4）与质膜结合，只有在照射后才能进入细胞，导致大量形态学改变。在用敏化剂处理过的细胞照射后，[Ca2+]i的增加与光量和细胞外[Ca2+]e有关。在没有[Ca2+]a的情况下，[Ca2+]i的增加显著减少。通过在高[Ca2+]e时增加[Ca2+]i，光动力治疗后的细胞损伤或死亡得到预防，并向更高的通量转移，而在低[Ca2+]e时损伤更大。应用Ca2+通道阻滞剂，如Co2+、Cd2+或维拉帕米，不能阻止[Ca2+]i的增加。我们的结果表明，光敏剂AIPcS4的激活导致Ca2+内流，从而保护细胞免受光损伤。在低[Ca2+]e和高通量值下，可能作为一种保护措施，内部储存的Ca2+释放，以增加[Ca2+]i。
