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Neuroprotector effect of p , p '‐methoxyl‐diphenyl diselenide in a model of sporadic dementia of Alzheimer's type in mice: contribution of antioxidant mechanism
Author(s) -
Pinton Simone,
da Rocha Juliana Trevisan,
Gai Bibiana Mozzaquatro,
Prigol Marina,
da Rosa Luiz Vinícius,
Nogueira Cristina Wayne
Publication year - 2011
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1741
Subject(s) - antioxidant , diphenyl diselenide , neuroprotection , streptozotocin , glutathione , chemistry , pharmacology , superoxide dismutase , endocrinology , medicine , dementia , biochemistry , diabetes mellitus , enzyme , disease , selenium , organic chemistry
The present study investigated whether the antioxidant activity of p , p '‐methoxyl‐diphenyl diselenide [(MeOPhSe) 2 ] is involved in its protective effect against cognitive impairment induced by streptozotocin (STZ) in a model of sporadic dementia of Alzheimer's type (SDAT). Swiss mice were treated with STZ or vehicle [2 µl of 2·5 mg ml −1 solution; intracerebroventricularly (i.c.v.)] twice, 48 h apart. (MeOPhSe) 2 (25 mg kg −1 ) or vehicle was orally administered 30 min prior to each STZ treatment. Neuroprotector effect of (MeOPhSe) 2 on the behavioral performance of mice on spatial recognition memory consolidation was investigated in the Y‐maze test. After that, mouse brains were removed for measuring antioxidant parameters. (MeOPhSe) 2 protected against the impairment in learning and memory caused by i.c.v. administration of STZ in mice. (MeOPhSe) 2 protected against the increase in reactive species and the reduction of glutathione levels, as well as, the increase in superoxide dismutase and glutathione S‐transferase activities caused by STZ in whole brain. These results suggest that antioxidant property is involved, at least in part, in the neuroprotective effect of (MeOPhSe) 2 on SDAT induced by STZ in mice. Copyright © 2011 John Wiley & Sons, Ltd.