Miyachi Y, Imamura S, Niwa Y, Tokura Y, Takigawa M
J Invest Dermatol. 1986 Jan;86(1):26-8. doi: 10.1111/1523-1747.ep12283753.
To investigate the possible participation of oxygen intermediates (OIs) in the contact photosensitization process, mice were treated with long-acting liposomal-superoxide dismutase (L-SOD) before photosensitization. Photosensitization to 3,3',4',5-tetrachlorosalicylanilide (TCSA) was significantly suppressed by the pretreatment of mice with L-SOD. This suppression was not mediated by suppressor cells or due to an unresponsive state produced by the use of L-SOD. Rather, the suppression appeared to be due to the failure of production of photoallergen. L-SOD treatment induced the suppression of contact photosensitivity to TCSA but not ordinary contact sensitivity to TCSA or dinitrofluorobenzene, suggesting that the production of photoallergen is more critically dependent on the presence of OIs than that of ordinary contact allergen. The results provide evidence that OIs are produced by light absorption in the presence of oxygen and react with the biologic substrate to form photoallergens.
为研究氧中间体(OIs)在接触性光敏化过程中可能的参与情况,在光敏化之前用长效脂质体超氧化物歧化酶(L-SOD)处理小鼠。用L-SOD预处理小鼠后,对3,3',4',5-四氯水杨酰苯胺(TCSA)的光敏化作用被显著抑制。这种抑制作用不是由抑制细胞介导的,也不是由于使用L-SOD产生的无反应状态。相反,这种抑制似乎是由于光变应原产生失败。L-SOD处理诱导了对TCSA接触性光敏反应的抑制,但对TCSA或二硝基氟苯的普通接触敏感性没有抑制作用,这表明光变应原的产生比普通接触性变应原的产生更关键地依赖于OIs的存在。结果提供了证据,即OIs是在有氧存在的情况下通过光吸收产生的,并与生物底物反应形成光变应原。