Inability to produce a model of dialysis encephalopathy in the rat by aluminum administration |
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Authors: | Thomas L Perry Voon Wee Yong William J Godolphin Michelle Sutter Shirley Hansen Stephen J Kish James G Foulks Masatoshi Ito |
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Institution: | (1) Department of Pharmacology & Therapeutics, The University of British Columbia, V6T 1W5 Vancouver, Canada;(2) Department of Pathology, The University of British Columbia, V6T 1W5 Vancouver, Canada;(3) Clarke Institute of Psychiatry, Toronto, Canada |
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Abstract: | We attempted to produce a rat model of brain aluminum toxicity in order to explore whether or not aluminum accumulation produces the neurochemical changes observed in brains of patients who die with dialysis encephalopathy. Daily subcutaneous injection of Al(OH)3 caused marked elevation of serum aluminum concentrations, but did not increase brain aluminum contents, either in rats with normal renal function, or in rats with unilateral or 5/6 nephrectomies. LiCl pretreatment, which has been reported to cause irreversible renal failure, did not impair renal function nor aid in achieving elevated brain aluminum contents. No reductions in brain contents of -aminobutyric acid (GABA) or in glutamic acid decarboxylase (GAD, E.C.4.1.1.15) and choline acetyltransferase (ChAT, E.C.2.3.1.6) activities were observed in aluminum-treated rats. We conclude that the rat is not a suitable laboratory animal to explore the role of aluminum toxicity in causing the GABA and ChAT deficits present in brains of hemodialyzed human patients. |
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Keywords: | Dialysis encephalopathy aluminum toxicity brain -aminobutyric acid" target="_blank">gif" alt="gamma" align="MIDDLE" BORDER="0">-aminobutyric acid |
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