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KMID : 0377519870120030361
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Chung-Ang Journal of Medicine
1987 Volume.12 No. 3 p.361 ~ p.379
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Effects of Iron Chelators and Reducing Agents on Iron induced Lipid Peroxidation
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Park, Chan-Hyun/박찬현
Lee, Chung-Soo/Shin, Yong-Kyu/Lee, Kwang-Soo/이정수/신용규/이광수
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Abstract
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Iron is a reactive metal ion which is known to catalyze damages of cellular macromolecules caused by oxygen radicals and its reduction may play a major role in lipid peroxidation. The iron-catalyzed Haber-Weiss reaction to produce OH- is catalyzed by iron and OH
appear to participate as an initiator of lipid peroxidation. Ferrous(or chelated) ion will also initiate peroxidation of unsaturated fatty
`{-´ acids. This initiation may occur via abstraction
hF by a ferrous-dioxygen complex or alternatively
s may involve 02, H2O, or other partially reduced oxygen species generated through fur-they autoxidation reactions of the ferrous chelates.1an3r studies have reported toxic effects of -.scorbate on various biological materials including lipid and DNA peroxidation. In view of data suggesting that the effect of iron on lipid peroxidation is mediated by its oxidoreduction, reducing activity of reducing agents such as ascorbate may be the mechanism through which the toxic action of ascorbate is mediated.
In the present study, the effect of oxidoreduction of iron on tissue damages was investigated in the presence of various reducing agents or iron chelators. These effects were
s:
studied with respect to generation of oxygenradicals during oxidation or reduction of iron in relation to the lipid peroxidation caused by iron. The effects of reducing agents or iron chelators on redox phenomenon of iron were also observed. Furthermore, the relationship between oxidoreduction - of iron and lipid , peroxidation was studied. Lipid peroxidation of microsomes was increased with concentration of Fell, but Fe+++ had little effect. In reaction medium of pH 7.4, Fell was ´almost completely autoxidized at 5 min after the reaction and during this process superoxide radical was formed. Lipid peroxidation of microsomes by Fell was inhibited by SOD and catalase. EDTA or DETAPAC showed dual effects on lipid peroxidation by Fell. When proportion of these chelators to iron was I 2, lipid peroxidation was enhanced but when this ratio is altered, lipid peroxidation was inhibited. ADP prevented lipid peroxidation by Fell and stimulated that by Fell´. EDTA or ADP facilitated autoxidation of Fell whereas DETAPAC inhibited. On the other hand, when proportion of EDTA or DETAPAC to Fell was 1 : 2, hydroxylation of sodium salicylate was maximum and fell off as this `proportion was altered. ADP also prevented hydroxylation of salicylate by Fell. Among various reducing agents tested ascorbate had a most potent reducing power and also most remarkably facilitated lipid peroxidation by iron. Lipid peroxidation caused by interaction of Fell and ascorbate was greater than that by interaction of Fell plus ascorbate. Reduction of ferricytochrome c was enhanced by ascorbate in a dose dependent manner, but other reducing agents showed little effect. Reduction of ferricytochcome c by Fell alone or Fell plus ascorbate was signifi cantly inhibited by SOD. However, reduction of ferricytochrome c by ascorbate alone was slightly inhibited by SOD. From these results obtained, it is suggested that
oxidoreduction of iron plays the major role in tissue damages including lipid peroxidation caused by iron dependent reactions and there is the relationship between the oxidoreduction of iron´ and lipid peroxidation. Also, it appears that oxygen radicals such as OH plays at least a partial role in initiating lipid peroxidation.
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