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In vivo and in vitro effects of homocysteine on Na + ,K + ‐ATPase activity in parietal, prefrontal and cingulate cortex of young rats
Author(s) -
Matté Cristiane,
Monteiro Siomara C.,
Calcagnotto Thiago,
Bavaresco Caren S.,
Netto Carlos Alexandre,
Wyse Angela T.S.
Publication year - 2004
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2004.05.007
Subject(s) - homocysteine , endocrinology , medicine , chemistry , oxidative stress , prefrontal cortex , in vivo , cingulate cortex , glutathione , cerebral cortex , thiobarbituric acid , biochemistry , lipid peroxidation , neuroscience , psychology , central nervous system , enzyme , biology , cognition , microbiology and biotechnology
In the present study we determined the effect of chronic administration of homocysteine on Na + ,K + ‐ATPase activity in synaptic membranes from parietal, prefrontal and cingulate cortex of young rats. We also studied the in vitro effect of homocysteine on this enzyme activity and on some oxidative stress parameters, namely thiobarbituric acid‐reactive substances (TBA‐RS) and total radical‐trapping antioxidant potential (TRAP) in the same cerebral structures. For the in vivo studies, we induced elevated levels of homocysteine in blood (500 μM), comparable to those of human homocystinuria, and in brain (60 nmol/g wet tissue) of young rats by injecting subcutaneously homocysteine (0.3–0.6 μmol/g of body weight) twice a day at 8 h intervals from the 6th to the 28th postpartum day. Controls received saline in the same volumes. Rats were killed 12 h after the last injection. Chronic administration of homocysteine significantly decreased (50%) Na + ,K + ‐ATPase activity in parietal, increased (36%) in prefrontal and did not alter in cingulate cortex of young rats. In vitro homocysteine decreased Na + ,K + ‐ATPase activity and TRAP and increased TBA‐RS in all cerebral structures studied. It is proposed that the alteration of Na + ,K + ‐ATPase and induction of oxidative stress by homocysteine in cerebral cortex may be one of the mechanisms related to the neuronal dysfunction observed in human homocystinuria.