作者: Saskia A.B.E. Van Acker , Dirk-jan Van Den Berg , MichÈl N.J.L. Tromp , Désirée H. Griffioen , Wout P. Van Bennekom
DOI: 10.1016/0891-5849(95)02047-0
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摘要: Flavonoids, a group of naturally occurring antioxidants and iron chelators, might be used as cardioprotective agents in doxorubicin-induced cardiotoxicity, which is believed to caused by the formation oxygen free radicals. To investigate underlying molecular mechanism, we tested large flavonoids from all major structural subclasses on their ability inhibit doxorubicin (enzymatically)-induced Fe2+/ascorbate (nonenzymatically)-induced microsomal lipid peroxidation (LPO) chelate Fe2+. In addition, measured half peak oxidation potentials (Ep/2). LPO inhibition data gave good qualitative correlation with potentials. Most chelated Fe2+, but there were differences chelating capacity. For scavenging activity, catechol moiety ring B required. The 3-OH can function chelation site also oxidized. combination C2 C3 double bond, increases activity. Fe2+ only plays role less active scavengers. Chelation then raise activity level most scavengers, possibly site-specific scavenging. It concluded that Ep/2 values almost completely describe inhibiting behaviour flavonoids.