Penning L C, Rasch M H, Ben-Hur E, Dubbelman T M, Havelaar A C, Van der Zee J, Van Steveninck J
University of Leiden, Sylvius Laboratory, Department of Medical Biochemistry, Netherlands.
Biochim Biophys Acta. 1992 Jun 30;1107(2):255-60. doi: 10.1016/0005-2736(92)90412-f.
Chinese hamster ovary (CHO) cells and T24 human bladder transitional carcinoma cells were treated with the photosensitizers aluminum phthalocyanine (AlPc) and hematoporphyrin derivative (HPD), respectively. Exposure of both sensitized cell lines to red light caused an immediate increase of cytoplasmic free calcium, [Ca2+]i, reaching a peak within 5-15 min after exposure and then returning to basal level (approximately 200 nM). The level of the peak [Ca2+]i depended on the light fluence, reaching a maximum of 800-1000 nM at light doses that kill about 90% of the cells. Loading the cells with the intracellular calcium chelators quin2 or BAPTA prior to light exposure enhanced cell killing. This indicates that increased [Ca2+]i after photodynamic therapy (PDT) contributed to survivability of the treated cells by triggering a cellular rescue response. The results of experiments with calcium-free buffer and calcium chelators indicate that both in CHO cells treated with AlPc and with HPD-PDT of T24 cells extracellular Ca2+ influx is mainly responsible for elevated [Ca2+]i. PDT is unique in triggering a cell rescue process via elevated [Ca2+]i. Other cytotoxic agents, e.g., H2O2, produce sustained increase of [Ca2+]i that is involved in the pathological processes leading to cell death.
分别用光敏剂铝酞菁（AlPc）和血卟啉衍生物（HPD）处理中国仓鼠卵巢（CHO）细胞和T24人膀胱移行癌细胞。使这两种致敏细胞系暴露于红光下会导致细胞质游离钙（[Ca2+]i）立即增加，在暴露后5 - 15分钟内达到峰值，然后恢复到基础水平（约200 nM）。[Ca2+]i的峰值水平取决于光通量，在杀死约90%细胞的光剂量下达到最大800 - 1000 nM。在光照前用细胞内钙螯合剂喹啉2或BAPTA加载细胞可增强细胞杀伤作用。这表明光动力疗法（PDT）后[Ca2+]i的增加通过触发细胞挽救反应促进了处理后细胞的存活能力。无钙缓冲液和钙螯合剂的实验结果表明，在用AlPc处理的CHO细胞和T24细胞的HPD - PDT中，细胞外Ca2+内流是[Ca2+]i升高的主要原因。PDT在通过升高[Ca2+]i触发细胞挽救过程方面是独特的。其他细胞毒性剂，例如H2O2，会使[Ca2+]i持续增加，这与导致细胞死亡的病理过程有关。
