Alteration of serum semicarbazide-sensitive amine oxidase activity in chronic renal failure

Despite recent intensive investigations, physiological and pathological role of semicarbazide-sensitive amine oxidase (SSAO) is far from clear. In this study, serum SSAO activity was determined, radiochemically, in various groups of uremic patients: haemodialysed (HD), peritoneally dialysed (PD) and...

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Published in:Journal of Neural Transmission 2007-06, Vol.114 (6), p.841-843
Main Authors: Nemcsik, J, Szökö, E, Soltész, Zs, Fodor, E, Toth, L, Egresits, J, Tábi, T, Magyar, K, Kiss, I
Format: Article
Language:English
Subjects:
Amine Oxidase (Copper-Containing) - analysis
Amine Oxidase (Copper-Containing) - blood
Biomarkers - analysis
Biomarkers - blood
Dialysis
Humans
Kidney - enzymology
Kidney - physiopathology
Kidney Failure, Chronic - blood
Kidney Failure, Chronic - enzymology
Kidney Failure, Chronic - physiopathology
Up-Regulation - physiology
Uremia - blood
Uremia - enzymology
Uremia - physiopathology
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Summary:Despite recent intensive investigations, physiological and pathological role of semicarbazide-sensitive amine oxidase (SSAO) is far from clear. In this study, serum SSAO activity was determined, radiochemically, in various groups of uremic patients: haemodialysed (HD), peritoneally dialysed (PD) and those receiving conservative treatment but still not dialysed (ND), as well as in controls. Reduced enzyme activity was found in HD uremic patients before and after dialysis treatment, compared to controls (5260 +/- 862 and 6011 +/- 958 pmol/h/ml vs. 8601 +/- 283 pmol/h/ml, p < 0.01 and p < 0.05, respectively). The activity was slightly lower in PD, and normal in ND patients. In HD patients SSAO activity was also determined by an assay based on the formation of hydrogen peroxide, and was found to be elevated compared to controls (2384 +/- 323 pmol/h/ml vs. 1437 +/- 72 pmol/h/ml, p < 0.05). The elevated serum SSAO activity measured through the detection of the enzyme-generated hydrogen peroxide in HD patients might indicate its contribution to the accelerated atherosclerotic disease observed in uremia.
ISSN:0300-9564
1435-1463
DOI:10.1007/s00702-007-0698-4