Affordable Access

Enzymatic defense against radiation damage in mice. Effect of selenium and vitamin E depletion.

Authors
  • Batist, G
  • Reynaud, A
  • Katki, A G
  • Travis, E L
  • Shoemaker, M C
  • Greene, R F
  • Myers, C E
Type
Published Article
Journal
Biochemical Pharmacology
Publisher
Elsevier
Publication Date
Feb 15, 1986
Volume
35
Issue
4
Pages
601–606
Identifiers
PMID: 3511917
Source
Medline
License
Unknown

Abstract

Radiation effects are mediated in part by the generation of oxygen-derived free radicals and hydrogen peroxide. Membrane polyunsaturated fatty acids are important biological targets of these toxic molecules which cause lipid peroxidation. Radiation damage to DNA is also known to result in base hydroperoxides, especially thymidine hydroperoxide. Glutathione (GSH) is known to inhibit lipid peroxidation both chemically and through its interaction with the selenium-dependent glutathione peroxidase (GSH-Px). Although cytosolic GSH-Px can metabolize organic lipid peroxides in solution, it cannot metabolize phospholipid peroxides in micelles. This may be due to the interference of phase differences between the aqueous cytosol and the membrane, or the result of steric hindrance. Recent studies have suggested the presence of a membrane-bound GSH-dependent peroxidase system. We examined the cytosolic versus membrane-associated GSH-Px, in various tissues of mice on a selenium and vitamin E deficient diet, and found significant differences among organs in the distribution of enzyme activity in these two subcellular fractions. The effect of single high-dose whole body irradiation did not appear to be related to the activity of these enzymes.

Report this publication

Statistics

Seen <100 times