Umemura S, Yumita N, Nishigaki R, Umemura K
Central Research Laboratory, Hitachi, Ltd., Tokyo.
Jpn J Cancer Res. 1990 Sep;81(9):962-6. doi: 10.1111/j.1349-7006.1990.tb02674.x.
The mechanism of cell damage by ultrasound in combination with hematoporphyrin was studied. Mouse sarcoma 180 cell suspensions were exposed to ultrasound for up to 60 s in the presence and absence of hematoporphyrin, with and without active oxygen scavengers. The cell damage enhancement by hematoporphyrin was suppressed by adding histidine but not by mannitol. The enhancement was doubled in rate by substitution of deuterium oxide medium for normal water. Sonoluminescence was produced in a saline solution under similar acoustic conditions and observed to have spectral components that can excite hematoporphyrin molecules. These results suggest that cell damage enhancement is probably mediated via singlet oxygen generated by ultrasonically activated hematoporphyrin.
研究了超声联合血卟啉对细胞损伤的机制。在有和没有血卟啉、有和没有活性氧清除剂的情况下，将小鼠肉瘤180细胞悬液暴露于超声长达60秒。添加组氨酸可抑制血卟啉对细胞损伤的增强作用，而甘露醇则无此作用。用重水介质替代普通水可使增强率加倍。在类似声学条件下，盐溶液中产生了声致发光，并观察到其光谱成分可激发血卟啉分子。这些结果表明，细胞损伤增强可能是通过超声激活血卟啉产生的单线态氧介导的。
