当前位置： SCI文献检索 > ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS期刊下所有文献 > Site-specific mechanisms of initiation by chelated iron and inhibition by alpha-tocopherol of lipid peroxide-dependent lipid peroxidation in charged micelles.

Site-specific mechanisms of initiation by chelated iron and inhibition by alpha-tocopherol of lipid peroxide-dependent lipid peroxidation in charged micelles.

Abstract：

:To obtain information on the role of iron-catalyzed lipid peroxidation in the presence of the small amount of lipid peroxide in deterioration of biological membranes, we examined factors affecting peroxidation of fatty acids in charged micelles. Peroxidation of linoleic acid (LA) was catalyzed by Fe2+ via reductive cleavage of linoleic acid hydroperoxide (LOOH) in negatively charged sodium dodecyl sulfate micelles, but not in positively charged tetradecyltrimethylammonium bromide (TTAB) micelles. However, this Fe2(+)-induced, LOOH-dependent lipid peroxidation could be induced in TTAB micelles in the presence of a negatively charged iron chelator, nitrilotriacetic acid (NTA). The linoleic acid alkoxy radical (LO.) generated by the LOOH-dependent Fenton reaction was also trapped by N-t-butyl-alpha-phenylnitrone at the surface of TTAB micelles in the presence of NTA, but not in its absence. The degradation rates of two spin probes, N-oxyl-4,4'-dimethyloxazolidine derivatives of stearic acid (5-NS and 16-NS), were investigated to determine the site of production of radicals formed during LOOH-dependent lipid peroxidation. The rate of consumption of 16-NS during the LOOH-dependent Fenton-like reaction was higher in TTAB micelles containing LA than in those containing lauric acid (LauA), although the rates of formation of LO. in the two types of fatty acid micelles were similar. The rates of 5-NS consumption in LA and LauA micelles were almost the same and were as low as that of 16-NS consumption in LauA micelles. 16-NS was more inhibitory than 5-NS of LOOH-dependent lipid peroxidation, and this inhibition was associated with its higher consumption of 16-NS than of 5-NS. alpha-Tocopherol inhibited NTA-Fe2(+)-induced LOOH-dependent lipid peroxidation in TTAB micelles, and was oxidized during this inhibition process. The rate and amount of alpha-tocopherol oxidized by the LOOH-dependent Fenton reaction were higher in LA micelles than in LauA micelles. alpha-Tocopherol inhibited the consumption of 16-NS during NTA-Fe2(+)-induced LOOH-dependent lipid peroxidation more effectively than that of 5-NS. The distribution of the chromanol moiety of alpha-tocopherol was studied by the fluorescence quenching method. There was no difference between Stern-Volmer plots of the quenchings of alpha-tocopherol fluorescence by 5-NS and 16-NS. From these results, we discuss the mechanism of induction of LOOH-dependent peroxidation of LA and the mechanism of the antioxidant effects of alpha-tocopherol on it from the viewpoint of site-specific reaction.

journal_name

Arch Biochem Biophys

journal_title

Archives of biochemistry and biophysics

authors

Fujii T,Hiramoto Y,Terao J,Fukuzawa K

doi

10.1016/0003-9861(91)90273-l

subject

Has Abstract

pub_date

1991-01-01 00:00:00

pages

120-6

issue

eissn

0003-9861

issn

1096-0384

pii

0003-9861(91)90273-L

journal_volume

284

pub_type

杂志文章

在线工具

Site-specific mechanisms of initiation by chelated iron and inhibition by alpha-tocopherol of lipid peroxide-dependent lipid peroxidation in charged micelles.