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Oxidative damages by iron‐chelate complexes depend on the interaction with the target molecules
Author(s) -
Asaumi Akira,
Ogino Tetsuya,
Akiyama Takashi,
Kawabata Teruyuki,
Okada Shigeru
Publication year - 1996
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549600201081
Subject(s) - chemistry , hydroxyl radical , nitrilotriacetic acid , citric acid , chelation , hydrogen peroxide , ferrous , medicinal chemistry , oxidative phosphorylation , autoxidation , nuclear chemistry , inorganic chemistry , radical , biochemistry , organic chemistry
To elucidate that in iron‐catalyzed oxidative damage the interaction of iron complex with the target molecules is important, the oxidative damage to plasmid DNA, protein and fatty acid has been compared using iron‐chelate complexes with nitrilotriacetic acid (nta), citric acid, ethylenediamine‐N,N′‐diacetic acid (edda) and diethylenetriamine‐N,N,N′,N″,N″‐pentaacetic acid (dtpa). In the presence of hydrogen peroxide, plasmid pBR322 strand breaks occurred in the order of Fe‐edda > Fe‐citrate > Fe‐nta >> Fe‐dtpa. However, fragmentation of bovine serum albumin and diene conjugation of linoleic acid micelle occurred in the order of Fe‐nta > Fe‐edda >> Fe‐citrate > Fe‐dtpa = 0, which were similar to hydroxyl radical production by these iron complexes and H2O2. Bleomycin‐detectable free radical‐promoting irons in these iron complexes were about 85% of iron in Fe‐nta, Fe‐citrate and Fe‐edda, and only about 33% in Fe‐dtpa. Not only hydroxyl radical productivity and free radical‐promoting iron content in iron complex, but also the interaction of the complex with the target molecules determines the iron‐catalyzed oxidative damage.