title: Protection by estrogens of biological damage by 2,2'-azobis(2-amidinopropane) dihydrochloride.
abstract: 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.
authors.affiliation: Department of Biochemistry, Hokkaido College of Pharmacy, Katuraoka-cho 7-1, Otaru 047-0264, Japan.
authors.forename: Sanae
authors.initials: S
authors.lastname: Muraoka
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Miura
mesh_terms: D000578:Amidines / Q000633:toxicity*; D000975:Antioxidants / Q000494:pharmacology; D016718:Arachidonic Acid / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects; D004578:Electron Spin Resonance Spectroscopy; D004958:Estradiol / Q000031:analogs & derivatives* / Q000494:pharmacology; D002393:Estrogens, Catechol / Q000494:pharmacology*; D016166:Free Radical Scavengers / Q000494:pharmacology*; D005609:Free Radicals / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D009113:Muramidase / Q000037:antagonists & inhibitors / Q000378:metabolism; D009153:Mutagens / Q000633:toxicity*; D010084:Oxidation-Reduction; D010100:Oxygen / Q000378:metabolism; D010545:Peroxides / Q000378:metabolism*; D010799:Phycoerythrin / Q000737:chemistry; D010957:Plasmids
chemical_list: D000578:Amidines; D000975:Antioxidants; D002393:Estrogens, Catechol; D016166:Free Radical Scavengers; D005609:Free Radicals; D009153:Mutagens; D010545:Peroxides; D010799:Phycoerythrin; D016718:Arachidonic Acid; C049375:perhydroxyl radical; D004958:Estradiol; C046728:2,2'-azobis(2-amidinopropane); C001390:2-hydroxyestradiol; C014036:4-hydroxyestradiol; D009113:Muramidase; D010100:Oxygen