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KMID : 0377519910160010035
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Chung-Ang Journal of Medicine
1991 Volume.16 No. 1 p.35 ~ p.47
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The Protective Acations of Ascorbate and Thiol Compounds in Lipid Peroxidation by Cu^(++)and H₂O₂
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Lee, Bok-Sang/이복상
Lee, Chung-Soo/Shin, Yong-Kyoo/Lee, Kwang-Soo/이정수/신용규/이광수
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Abstract
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Copper has been suggested to facilitate the oxidative tissue injuries through the formation of either reactive oxygen radicals or cupuryl peroxide ion. The reducing agents including glutathione are known to inhibit the oxygen metabolites-induced cytotoxicity. In the present study, the effects of ascorbate, NADH and thiol compounds on lipid peroxidation caused by Cu" and H2O2 were investigated. The oxidations of ascorbate, NADH and glutathione in the presence of Cu" and H2O2, and the decomposition of were observed.
Lipid peroxidation of microsomes was enhanced by addition of Cu" and H2O2 with incubation time, and this was greater than the summation of effects of Cu" alone and H2O2 alone. The Cu" and H2O2-induced lipid peroxidation was inhibited by catalase and slightly inhibited by DMSO, but not affected by SOD, mannitol and DABCO. H2O2 was decomposed by Cu". Lipid peroxidations by Cu" plus H2O2, Cu" alone and H2O2 alone were all inhibited by NADH, glutathione, MPG and cystein. On the other hand, ascorbate inhibited the peroxidative action of Cu" plus H2O2 but stimulated that of either Cu" alone or H2O2 alone. The oxidations of ascorbate, NADH and glutathione were markedly stimulated by addition of Cu" iplus H2O2 and the stimulatory actions of Cu" plus H2O2 were greater than that of either Cu" alone or H2O2 alone. Cu" plus H202-induced oxidation of ascorbate was inhibited by catalase but not affected by DMSO. Lipid peroxidation by Fe" plus
Dc Ell
H2O2 was markedly stimulated by ascorb; i t~ but inhibited by glutathione. These result, suggest that lipid peroxidation caused b` Cu" plus H2O2 may be attributable to
complex of Cu" and H2O2 rather than ox ygen radicals. The oxidation itself of reduc ing agent may play a role in the protection for the oxidative tissue injury by a Cu++-H20 complex.
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