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Ascorbate Inhibits Edema in Brain Slices
Author(s) -
Brahma B.,
Forman R.E.,
Stewart E.E.,
Nicholson C.,
Rice M.E.
Publication year - 2000
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2000.741263.x
Subject(s) - chemistry , nmda receptor , ascorbic acid , glutamate receptor , intracellular , biophysics , biochemistry , antioxidant , forebrain , receptor , endocrinology , biology , central nervous system , food science
Ascorbate is an essential antioxidant in the CNS, localized predominantly in neuronal cytosol. Slices of mammalian brain rapidly lose ascorbate, however, when incubated in ascorbate‐free media; brain slices also take up water and swell. Here we investigated water gain in coronal slices of rat forebrain incubated with and without ascorbate for 1‐3 h at 34°C. Slices progressively gained water in ascorbate‐free media, with a significant 12% water increase after 3 h at 34°C, compared with the water content of slices after a 1‐h recovery period at 24°C, immediately following slice preparation. Inclusion of 400 μ M ascorbate in the medium led to an increase in tissue ascorbate content and prevented water gain at 34°C. By contrast, water gain was not inhibited by isoascorbate or thiourea, which are antioxidants that are not accumulated in brain cells. The oxidant H 2 O 2 enhanced water gain, whereas a cocktail of NMDA and non‐NMDA receptor blockers inhibited edema formation to the same extent as ascorbate. These data demonstrate that brain edema, linked to glutamate‐receptor activation, can result from intracellular oxidative stress and that this can be prevented by ascorbate.