Abstract |
Lipid peroxidation of rat liver microsomal fractions was monitored by its low-level chemiluminescence in preparations from controls and vitamin-E-deficient animals. Measurements were made (a) of the duration of the lag phase tau0 after initiation with NADPH/ iron- ADP and (b) of the slope of the chemiluminescence increase. In microsomes with normal vitamin E ( alpha-tocopherol) level the lag phase tau0 was substantially increased by ascorbate; in contrast, even an enhanced peroxidation was observed with ascorbate in vitamin-E-deficient microsomes. Therefore, the ascorbate-mediated protection of microsomal membranes against lipid peroxidation is dependent on vitamin E in the membrane. In vitamin E deficiency the pro-oxidant effect of ascorbate was abolished when glutathione (GSH) was present. Likewise, GSH does not prolong the lag phase tau0 in vitamin E deficiency. However, GSH (but not cysteine) exerts an antioxidant effect both in controls and in vitamin E deficiency by decreasing the slope of the chemiluminescence increase during lipid peroxidation. The involvement of GSH in an enzyme-dependent mechanism is suggested.
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Authors | H Wefers, H Sies |
Journal | European journal of biochemistry
(Eur J Biochem)
Vol. 174
Issue 2
Pg. 353-7
(Jun 01 1988)
ISSN: 0014-2956 [Print] England |
PMID | 3383850
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Lipid Peroxides
- Sulfhydryl Compounds
- Vitamin E
- Glutathione
- Cysteine
- Ascorbic Acid
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Topics |
- Animals
- Ascorbic Acid
(pharmacology)
- Cysteine
(pharmacology)
- Glutathione
(pharmacology)
- Lipid Peroxides
(biosynthesis)
- Luminescent Measurements
- Microsomes, Liver
(metabolism)
- Rats
- Sulfhydryl Compounds
(pharmacology)
- Vitamin E
(pharmacology)
- Vitamin E Deficiency
(metabolism)
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