Chen Y Q, Wang J, Liu Y Z, Yu S Y
Zhonghua Zhong Liu Za Zhi. 1986 Nov;8(6):413-6.
Ascitic hepatoma cells of mice were incubated with three HPD. After the cell-bound HPD was treated by visible light, the product of membrane lipid peroxidation--malondialdehyde (MDA) was determined. The results showed that the MDA level increased with HPD concentration and exposure time, but it was unchanged in the control. Beta-carotene, a quencher of singlet oxygen, could inhibit the lipid photooxidation of the membrane of cell-bound HPD resulting in a decrease of MDA level which decreased with increase of beta-carotene concentration. Adding vitamin E in vitro and vivo, formation of the product of membrane lipid peroxidation of cell-bound HPD by light was inhibited and the MDA level decreased with the increase of vitamin E concentration. These results show that the singlet oxygen, produced by HPD bound cells following light activation, reacts directly with the polyunsaturated fatty acids on cell membrane to produce lipid peroxides leading to cellular damage.
将小鼠腹水肝癌细胞与三种血卟啉衍生物(HPD)一起孵育。在用可见光处理结合细胞的HPD后,测定膜脂质过氧化产物——丙二醛(MDA)。结果显示,MDA水平随HPD浓度和照射时间的增加而升高,但在对照组中无变化。单线态氧猝灭剂β-胡萝卜素可抑制结合细胞的HPD膜的脂质光氧化,导致MDA水平降低,且MDA水平随β-胡萝卜素浓度的增加而降低。在体外和体内添加维生素E,可抑制结合细胞的HPD经光照后膜脂质过氧化产物的形成,且MDA水平随维生素E浓度的增加而降低。这些结果表明,光激活后结合细胞的HPD产生的单线态氧直接与细胞膜上的多不饱和脂肪酸反应,生成脂质过氧化物,导致细胞损伤。