Wennersten G, Brunk U
Acta Derm Venereol. 1978;58(4):297-305.
A recent report described the establishment of an experimental model for studying photo-oxidative damage inflicted by kynurenic acid on cultivated cells. Preliminary findings by scanning electron microscopy (SEM) were reported. For the present paper supplementary SEM studies were performed, and it was found that maximum cell damage appears 2 to 4 hours post irradiation. With low concentrations of kynurenic acid and brief UVA exposure, repair mechanisms seem to occur. Damage in the form of cellular swelling and plasma membrane alterations is most easily recognized by SEM, which is far more sensitive than ordinary light microscopy. Transmission electron microscopy (TEM) reveals morphologic alterations, consisting of an enhanced formation of endocytotic vacuoles from the plasma membranes, swelling with disruptions of the cell sap continuity, mitochondrial swelling, dilatation of the endoplasmic net, and vesiculation of some of the microvilli. Lysosomal damage, which was not seen until very late post irradiation and only for high concentrations of kynurenic acid and long-term UVA exposure, seems to be a secondary phenomenon. This hypothesis is further supported by the cytochemical analysis. The primary event thus seems to affect the plasma membrane level and originate in the binding of kynurenic acid to the plasma membrane on which subsequent UVA irradiation inflicts secondary intracellular alterations due to increased permeability and swelling.
最近的一份报告描述了一种用于研究犬尿氨酸对培养细胞造成光氧化损伤的实验模型的建立。报告了通过扫描电子显微镜（SEM）得出的初步结果。在撰写本文时进行了补充性的SEM研究，发现最大细胞损伤出现在照射后2至4小时。使用低浓度的犬尿氨酸并进行短暂的紫外线A（UVA）照射时，似乎会出现修复机制。细胞肿胀和质膜改变形式的损伤通过SEM最容易识别，SEM比普通光学显微镜敏感得多。透射电子显微镜（TEM）揭示了形态学改变，包括质膜内吞泡形成增加、细胞液连续性中断导致肿胀、线粒体肿胀、内质网扩张以及一些微绒毛形成小泡。溶酶体损伤直到照射后很晚才出现，且仅在高浓度犬尿氨酸和长期UVA照射时才出现，似乎是一种继发现象。这一假设得到了细胞化学分析的进一步支持。因此，主要事件似乎影响质膜水平，起因是犬尿氨酸与质膜结合，随后UVA照射由于通透性增加和肿胀导致细胞内继发改变。
