EFFECT OF TERT-BUTYL HYDROPEROXIDE ADDITION ON SPONTANEOUS CHEMILUMINESCENCE IN BRAIN

Citation
I. Azorin et al., EFFECT OF TERT-BUTYL HYDROPEROXIDE ADDITION ON SPONTANEOUS CHEMILUMINESCENCE IN BRAIN, Free radical biology & medicine, 19(6), 1995, pp. 795-803
Citations number
38
Categorie Soggetti
Biology
ISSN journal
08915849
Volume
19
Issue
6
Year of publication
1995
Pages
795 - 803
Database
ISI
SICI code
0891-5849(1995)19:6<795:EOTHAO>2.0.ZU;2-Z
Abstract
It is well known that light emission is related to lipid peroxidation in biological material, and that this process occurs spontaneously in the brain. tert-Butyl hydroperoxide (tBHP) is an organic peroxide wide ly used as initiator of free radical production in several biological systems. However, the prooxidant capacity of this compound remains unc lear. To clarify its role in brain spontaneous autooxidation, rat brai n homogenates were incubated with and without tBHP. Light emission and lipid peroxidation were measured by luminometry and the TBARs test, r espectively. Several inhibitors of free radical-induced lipid peroxida tion were also used. These inhibitors included ascorbate, EDTA, and de sferrioxamine. Our results indicate that the pattern of light emission spontanously produced in brain was different from that observed after the addition of tBHP to the homogenates, and that these differences d epended on the tBHP concentration. The main difference was that tBHP c aused a rapid light emission that reached its maximum more quickly tha n in the case of spontaneous emission. Addition of ascorbate resulted in an increase in chemiluminescence in presence of tBHP. In contrast, EDTA and desferrioxamine inhibited light emission in homogenates both with and without tBHP. The results of MDA determination were similar t o those described, including the effect of inhibitors. A common featur e in MDA and luminometric determinations was the dispersion of data. I n conclusion, these results suggest that tBHP, under specific conditio ns, modify the kinetic pattern of brain spontaneous autooxidation.