Chen Y Q
Cancer Institute, Chinese Academy of Medical Sciences, Beijing.
Zhonghua Zhong Liu Za Zhi. 1991 Jul;13(4):269-72.
Light-induced generation of hydrogen peroxide and hydroxyl free radical by HPD in the presence of ascorbate was studied. 1. Oxygen consumption was determined by oxygen electrodes when the HPD-ascorbate solution was illuminated. After the illumination, addition of 300 unit/ml of catalase to the illuminated HPD-ascorbate solution initiated a return of 20% of the oxygen. The results indicated the presence of H2O2 in the solution. 2. Ascitic hepatoma cells of mice, mitochondria and lysosomes were incubated with HPD, respectively and then were treated with ascorbate and light. The product of membrane lipid peroxidation-malondialdehyde (MDA) level was increased with the increase of ascorbate concentration and irradiation time. 3. Thiourea, an inhibitor of hydroxyl free radical, could inhibit the MDA produced in the cell-HPD-ascorbate and light system. The MDA level was inversely proportional to thiourea concentration. These results show that hydroxyl free radical produced by HPD-ascorbate and light could directly oxidize the membrane lipids, thus leading to enhancement of HPD photosensitization.
研究了在抗坏血酸存在下，血卟啉衍生物（HPD）光诱导产生过氧化氢和羟基自由基的情况。1. 当HPD-抗坏血酸溶液受到光照时，用氧电极测定耗氧量。光照后，向光照后的HPD-抗坏血酸溶液中加入300单位/毫升的过氧化氢酶，可使20%的氧恢复。结果表明溶液中存在过氧化氢。2. 将小鼠腹水肝癌细胞、线粒体和溶酶体分别与HPD孵育，然后用抗坏血酸和光照处理。膜脂质过氧化产物丙二醛（MDA）水平随抗坏血酸浓度和照射时间的增加而升高。3. 羟基自由基抑制剂硫脲可抑制细胞-HPD-抗坏血酸和光照体系中产生的MDA。MDA水平与硫脲浓度成反比。这些结果表明，HPD-抗坏血酸和光照产生的羟基自由基可直接氧化膜脂质，从而增强HPD的光敏作用。
