Muraoka Sanae, Miura Toshiaki
Department of Biochemistry, Hokkaido College of Pharmacy, Katuraoka-cho 7-1, Otaru 047-0264, Japan.
J Steroid Biochem Mol Biol. 2002 Nov;82(4-5):343-8. doi: 10.1016/s0960-0760(02)00216-9.
We examined by using 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) as a radical generator the ability of estrogens to scavenge carbon-centered and peroxyl radicals. Electron spin resonance signals of carbon-centered radicals from AAPH were diminished by catecholestrogens but not by phenolic estrogens, showing that catecholestrogens efficiently scavenged carbon-centered radicals. However, fluorescent decomposition of R-phycoerythrin by AAPH-derived peroxyl radicals was inhibited by catecholestrogens and phenolic estrogens. Evidently, peroxyl radicals were scavenged by catecholestrogens and by phenolic estrogens. However, the scavenging ability of 4-hydroxyestradiol was less than 2-hydroxyestradiol. Strand break of DNA induced by AAPH was inhibited by catecholestrogens, but not by phenolic estrogens under aerobic and anaerobic conditions. Inactivation of lysozyme induced by AAPH was completely blocked by 2-hydroxyestradiol under aerobic and anaerobic conditions, and by 4-hyroxyestradiol only under anaerobic conditions. Peroxidation of arachidonic acid by AAPH was strongly inhibited by catecholestrogens at low concentrations. Only large amounts of phenolic estrogens markedly inhibited lipid peroxidation. These results show that catecholestrogens were antioxidant against AAPH-induced damage to biological molecules through scavenging both carbon-centered and peroxyl radicals, but phenolic estrogens partially inhibited AAPH-induced damage because they scavenged only peroxyl radicals.
我们使用2,2'-偶氮二异丁脒二盐酸盐（AAPH）作为自由基发生器，研究了雌激素清除碳中心自由基和过氧自由基的能力。儿茶酚雌激素可使AAPH产生的碳中心自由基的电子自旋共振信号减弱，而酚类雌激素则不能，这表明儿茶酚雌激素能有效清除碳中心自由基。然而，AAPH衍生的过氧自由基对R-藻红蛋白的荧光分解受到儿茶酚雌激素和酚类雌激素的抑制。显然，过氧自由基可被儿茶酚雌激素和酚类雌激素清除。然而，4-羟基雌二醇的清除能力低于2-羟基雌二醇。在需氧和厌氧条件下，AAPH诱导的DNA链断裂受到儿茶酚雌激素的抑制，但不受酚类雌激素的抑制。在需氧和厌氧条件下，2-羟基雌二醇可完全阻断AAPH诱导的溶菌酶失活，而4-羟基雌二醇仅在厌氧条件下可完全阻断。低浓度的儿茶酚雌激素可强烈抑制AAPH诱导的花生四烯酸过氧化。只有大量的酚类雌激素能显著抑制脂质过氧化。这些结果表明，儿茶酚雌激素通过清除碳中心自由基和过氧自由基，对AAPH诱导的生物分子损伤具有抗氧化作用，而酚类雌激素仅通过清除过氧自由基部分抑制AAPH诱导的损伤。
