Determination of serum aluminum, platelet aggregation and lipid peroxidation in hemodialyzed patients
Aluminum (Al3+) overload is frequently associated with lipid peroxidation and neurological disorders. Aluminum accumulation is also reported to be related to renal impairment, anemia and other clinical complications in hemodialysis patients. The aim of the present study was to determine the degree o...
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Published in: | Brazilian journal of medical and biological research Vol. 35; no. 3; pp. 345 - 350 |
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Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Brazil
Associação Brasileira de Divulgação Científica
01-03-2002
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Subjects: | |
Online Access: | Get full text |
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Summary: | Aluminum (Al3+) overload is frequently associated with lipid peroxidation and neurological disorders. Aluminum accumulation is also reported to be related to renal impairment, anemia and other clinical complications in hemodialysis patients. The aim of the present study was to determine the degree of lipid peroxidation, platelet aggregation and serum aluminum in patients receiving regular hemodialytic treatment. The level of plasma lipid peroxidation was evaluated on the basis of thiobarbituric acid reactive substances (TBARS). Mean platelet peroxidation in patients undergoing hemodialysis was significantly higher than in normal controls (2.7 +/- 0.03 vs. 1.8 +/- 0.06 nmol/l, P<0.05). Platelet aggregation and serum aluminum levels were determined by a turbidimetric method and atomic absorption spectrophotometry, respectively. Serum aluminum was significantly higher in patients than in normal controls (44.5 +/- 29 vs. 10.8 +/- 2.5 microg/l, P<0.05). Human blood platelets were stimulated with collagen (2.2 microg/ml), adenosine diphosphate (6 microM) and epinephrine (6 microM) and showed reduced function with the three agonists utilized. No correlation between aluminum levels and platelet aggregation or between aluminum and peroxidation was observed in hemodialyzed patients. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0100-879X 1414-431X 0100-879X 1414-431X |
DOI: | 10.1590/S0100-879X2002000300009 |