Shea C R, Whitaker D, Murphy G F, Hasan T
Wellman Laboratories of Photomedicine, Massachusetts General Hospital, Harvard Medical School, Boston 02114.
Am J Pathol. 1988 Nov;133(2):381-8.
Mechanisms and intracellular sites of photosensitized damage were investigated in cultured MGH-U1 cells treated with doxycycline (DOTC). Cells were examined by phase-contrast, fluorescence, and electron microscopy at various times (15 minutes to 24 hours) after ultraviolet irradiation (320-400 nm). DOTC localized selectively within the mitochondria, as shown by colocalized fluorescence with rhodamine 123 (R123). Photosensitization at 1 J/sq cm caused striking swelling of the mitochondrial matrix and disruption of the cristae, accompanied by loss of the ability of mitochondria to concentrate R123. These changes progressed during the first hour after irradiation, and then were followed by partial recovery of mitochondrial ultrastructure and function. At no time were other organelles seen to be affected. It appears that this selective, photosensitized alteration was a consequence of localized and partially reversible damage to the mitochondrial inner membrane. In contrast, exposure to 2-6 J/sq cm caused irreversible injury and necrosis.
在用强力霉素（DOTC）处理的培养MGH-U1细胞中研究了光致敏损伤的机制和细胞内位点。在紫外线照射（320 - 400纳米）后的不同时间（15分钟至24小时），通过相差显微镜、荧光显微镜和电子显微镜对细胞进行检查。如与罗丹明123（R123）的共定位荧光所示，DOTC选择性地定位于线粒体内。1焦耳/平方厘米的光致敏导致线粒体基质显著肿胀和嵴破坏，同时线粒体浓缩R123的能力丧失。这些变化在照射后的第一小时内进展，随后线粒体超微结构和功能部分恢复。在任何时候都未观察到其他细胞器受到影响。看来这种选择性的光致敏改变是线粒体内膜局部且部分可逆损伤的结果。相比之下，暴露于2 - 6焦耳/平方厘米会导致不可逆损伤和坏死。
