TEMPERATURE-DEPENDENT LIPID-PEROXIDATION OF RAT-BRAIN HOMOGENATE

Citation
T. Miura et al., TEMPERATURE-DEPENDENT LIPID-PEROXIDATION OF RAT-BRAIN HOMOGENATE, Research communications in molecular pathology and pharmacology, 100(1), 1998, pp. 117-128
Citations number
21
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology & Pharmacy",Pathology,Biology
ISSN journal
1078-0297
Volume
100
Issue
1
Year of publication
1998
Pages
117 - 128
Database
ISI
SICI code
1078-0297(1998)100:1<117:TLORH>2.0.ZU;2-B
Abstract
When rat brain homogenate was incubated without adding iron, lipid per oxidation occurred temperature dependently between 27 degrees C and 42 degrees C. When homogenates of liver and heart were incubated under t he same conditions, lipid peroxidation did not occur. The brain, compa red with other organs, seems to be very vulnerable to oxidative damage with fever. Catalase promoted lipid peroxidation. The ability of dihy drolipoic acid and alpha-tocopherol to inhibit lipid peroxidation was very weak. In contrast, iron chelators, such as bathophenanthroline, d esferrioxamine and EDTA, strongly inhibited lipid peroxidation, indica ting that endogenous iron is involved in lipid peroxidation, Dialysis of brain homogenate depressed the temperature-dependent lipid peroxida tion by about 30%. Then, the iron content of the homogenate decreased by about 35%. On the other hand, dialysis of EDTA-treated homogenate c ompletely depressed the lipid peroxidation and the iron content of the homogenate decreased by about 87%. Adding iron to the homogenate dial yzed after EDTA treatment remarkably increased the lipid peroxidation, but the peroxidation reaction proceeded temperature independently. Ou r results suggest that endogenous iron, which may bind to cell compone nts, causes temperature dependent lipid peroxidation by a site-specifi c mechanism.