Imai K, Aimoto T, Sato M, Kimura R
Faculty of Pharmaceutical Sciences, Setsunan University, Osaka, Japan.
Biol Pharm Bull. 1995 Jun;18(6):913-6. doi: 10.1248/bpb.18.913.
Antioxidative inhibition by protoporphyrin (PP) of peroxidative damage in lysosomes, mitochondria and microsomes of rat liver was investigated at 24 h after an intravenous administration of PP. Using a lysosome-containing (3500 x g) fraction, the release of lysosomal marker enzymes, acid phosphatase and aryl sulfatase, from lysosome which had been stimulated by L-ascorbic acid (AsA), was decreased dose-dependently, as was the inhibition of lipid peroxidation by PP in the fraction. Swelling of mitochondria induced by Fe2+ and AsA was also inhibited in the PP-injected rat. In microsomes, lipid peroxidation stimulated by AsA caused a decrease in activity of a microsomal marker enzyme, glucose 6-phosphatase, and in P450 content. The extent of the decrease by AsA, both in activity and content, was diminished in PP-administered rat liver microsomes. These results indicate that PP protects those subcellular fractions from deterioration by lipid peroxidation.
在静脉注射原卟啉（PP）24小时后，研究了原卟啉对大鼠肝脏溶酶体、线粒体和微粒体过氧化损伤的抗氧化抑制作用。使用含溶酶体的（3500×g）组分，由L-抗坏血酸（AsA）刺激的溶酶体中溶酶体标记酶酸性磷酸酶和芳基硫酸酯酶的释放呈剂量依赖性降低，该组分中PP对脂质过氧化的抑制作用也呈剂量依赖性降低。在注射PP的大鼠中，由Fe2+和AsA诱导的线粒体肿胀也受到抑制。在微粒体中，由AsA刺激的脂质过氧化导致微粒体标记酶葡萄糖6-磷酸酶的活性和P450含量降低。在给予PP的大鼠肝脏微粒体中，AsA引起的活性和含量降低的程度减小。这些结果表明，PP可保护这些亚细胞组分免受脂质过氧化的破坏。
