Open AccessGeneration of hydrogen peroxide by cerebral‐cortex synaptosomes
Author(s) -
ZOCCARATO Franco,
DEANA Renzo,
CAVALLINI Lucia,
ALEXANDRE Adolfo
Publication year - 1989
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1989.tb14670.x
Subject(s) - veratridine , synaptosome , chemistry , ionomycin , verapamil , glutathione , ionophore , depolarization , biophysics , cerebral cortex , calcium , hydrogen peroxide , guinea pig , biochemistry , medicine , membrane , endocrinology , sodium , enzyme , biology , intracellular , sodium channel , organic chemistry
Guinea‐pig cerebral cortex synaptosomes steadily release H 2 O 2 into the suspending medium, at the rate of 20–30 pmol min −1 mg protein −1 . A transient increase of the H 2 O 2 release is induced by the addition of 1 mM Ca 2+ , which declines within 60–90 s to a rate identical or slightly higher than that before Ca 2+ . The extra H 2 O 2 following Ca 2+ addition varies between 40–100 pmol/mg protein and is insensitive to verapamil. The H 2 O 2 release increases strongly (up to 250 pmol min −1 mg −1 ) upon depletion of the synaptosomal glutathione by treatment with 1‐chloro‐2,4‐dinitrobenzene, a substrate for glutathione transferase. This treatment however has no effect on the Ca 2+ ‐induced H 2 O 2 transient. In these treated synaptosomes a further increase of the output of H 2 O 2 is rapidly induced upon addition of the Ca 2+ ionophore ionomycin. This increase (about 100 pmol min −1 mg −1 ) lasts several minutes and requires the presence of Ca 2+ . A similar, though less pronounced increased H 2 O 2 release is obtained (also in the absence of Ca 2+ ) upon depolarization of the synaptosomal plasma membrane with KCI or with veratridine.