Ohmori Sayaka, Masuda Kensuke, Yoshida Masatake, Arai Tsunenori, Nakajima Susumu
School of Fundamental Science and Technology, Graduate School of Science and Technology, Keio University, 3-14-1 Hiyoshi, Kouhoku-ku, Yokohama 223-8522, Japan.
Lasers Med Sci. 2005 Sep;20(2):54-61. doi: 10.1007/s10103-005-0342-1. Epub 2005 Jul 9.
We studied hydrophilic photosensitizer ATX-S10Na(II) mediated photocytotoxicity against macrophage-like cell under pulsed irradiation. We found that photocytotoxicity suppression under high intensity irradiation was directly induced by a decrease in the Type-II photoreaction. We showed that this decrease was not attributable to absorption saturation with the high intensity irradiation. We found the cell lethality change from 70% to 13% with the pulse peak power density ranging from 0.29 MW/cm(2) to 1.36 MW/cm(2), at the light dose of 20 J/cm(2) and the pulse repetition rate at 40 Hz. To investigate the Type-II reaction, we measured the photobleaching, oxygen consumption and singlet oxygen luminescence of the photosensitizer solution. The transient absorption from the photosensitizer during the irradiation was measured with the pump-and-probe technique. We believe that the photocytotoxicity suppression induced by the high intensity irradiation might be useful for the treatment of depth-controlled photodynamic therapy without the wall damage of a hollow organ.
我们研究了亲水性光敏剂ATX-S10Na(II)在脉冲照射下对巨噬细胞样细胞的光细胞毒性。我们发现，高强度照射下的光细胞毒性抑制是由II型光反应的降低直接诱导的。我们表明，这种降低并非归因于高强度照射下的吸收饱和。我们发现，在光剂量为20 J/cm(2)、脉冲重复频率为40 Hz时，随着脉冲峰值功率密度从0.29 MW/cm(2)变化到1.36 MW/cm(2)，细胞致死率从70%变为13%。为了研究II型反应，我们测量了光敏剂溶液的光漂白、耗氧量和单线态氧发光。用泵浦-探测技术测量了照射期间光敏剂的瞬态吸收。我们认为，高强度照射诱导的光细胞毒性抑制可能有助于在不损伤中空器官壁的情况下进行深度可控的光动力治疗。
