Role of iron, zinc and reduced glutathione in oxidative stress induction by low pH in rat brain synaptosomes

Brain ischemia leads to a decrease in pH o . We have shown previously in synaptosomes that the extracellular acidification induces depolarization of mitochondria followed by synthesis of superoxide anions and oxidative stress. Here, we investigated the effects of lowered pH o on oxidative stress and...

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Bibliographic Details
Published inSpringerPlus Vol. 3; no. 1; p. 560
Main Authors Pekun, Tatyana G., Hrynevich, Sviatlana V., Waseem, Tatyana V., Fedorovich, Sergei V.
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 26.09.2014
Springer Nature B.V
BioMed Central Ltd
Subjects
Biomedical and Life Sciences
Humanities and Social Sciences
Molecular Neuroscience
multidisciplinary
Science
Science (multidisciplinary)
Iron
Synaptosomes
Acidosis, ischemia
Zinc
Glutathione
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Summary:Brain ischemia leads to a decrease in pH o . We have shown previously in synaptosomes that the extracellular acidification induces depolarization of mitochondria followed by synthesis of superoxide anions and oxidative stress. Here, we investigated the effects of lowered pH o on oxidative stress and membrane potentials in synaptosomes treated by the iron chelator deferoxamine and zinc chelator TPEN. We demonstrated that chelating of metals has no impact on superoxide anion synthesis and intrasynaptosomal mitochondria depolarization. Meanwhile, deferoxamine was able to inhibit oxidative stress induced by low pH o and hydrogen peroxide application. Compared to deferoxamine, TPEN was less effective but it decreased the DCF fluorescence induced by pH o 6.0 which had no effects in other oxidative stress models. We found that the chelators were able to inhibit slightly plasma membrane depolarization. Synaptosomes preincubation at low pH o caused no effects on the reduced glutathione level. Depletion of glutathione by CDNB produced no additional increase in the DCF fluorescence induced by pH o 7.0. Our results suggest that free iron is crucial for the development of oxidative stress elicited by acidification in synaptosomes. Chelating of this metal seems to be a promising strategy for protecting the neuronal presynaptic terminals against oxidative stress developed at stroke.
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ISSN:2193-1801
2193-1801
DOI:10.1186/2193-1801-3-560