Korean J Physiol Pharmacol.
1997 Aug;1(4):367-376.
Effect of t-butylhydroperoxide on Na+/-dependent glutamate uptake in
rabbit brain synaptosome
- Affiliations
-
- 1Department of Physiology, College of Medicine, Pusan National University,
Pusan 602-739, Korea.
Abstract
-
The effect of an organic peroxide, t-butylhydroperoxide (t-BHP), on
glutamate uptake was studied in synaptosomes prepared from cerebral
cortex. t-BHP inhibited the Na+/-dependent glutamate uptake with no
change in the Na+/-independent uptake. This effect of t-BHP was not
altered by addition of Ca2+ channel blockers (verapamil, diltiazem and
nifedipine) or PLA2 inhibitors (dibucaine, butacaine and quinacrine).
However, the effect was prevented by iron chelators (deferoxamine and
phenanthroline) and phenolic antioxidants
(N,N'-diphenyl-phenylenediamine, butylated hydroxyanisole, and
butylated hydroxytoluene). At low concentrations (< 1.0 mM), t-BHP
inhibited glutamate uptake without altering lipid peroxidation.
Moreover, a large increase in lipid peroxidation by ascorbate/Fe2+ was
not accompanied by an inhibition of glutamate uptake. The impairment of
glutamate uptake by t-BHP was not intimately related to the change in
Na+/-K+/-ATPase activity. These results suggest that inhibition of
glutamate uptake by t-BHP is not totally mediated by peroxidation of
membrane lipid, but is associated with direct interactions of glutamate
transport proteins with t-BHP metabolites. The Ca2+ influx through Ca2+
channel or PLA2 activation may not be involved in the t-BHP inhibition
of glutamate transport.