Metabolism - Clinical and Experimental
Volume 45, Issue 11 , Pages 1319-1322, November 1996

Protein oxidation in hemodialysis and kidney transplantation

Department of Internal Medicine and Institute of General Pathology, University of Genoa, Genoa, Italy

Received 26 June 1995; accepted 9 June 1996.

Abstract 

Oxidative damage of plasma proteins determined with the markers carbonyl group (CG) content and thiobarbituric acid—reactive substances (TBARS) was studied in 13 hemodialyzed and eight kidney-transplanted patients. The level of CGs was 38% higher in hemodialysis (HD) patients (1.49 ± 0.05 nmol/mg protein) than in the healthy subjects (1.08 ± 0.03 nmol/mg protein); the TBARS level was also higher in HD patients than in the control group (2.64 ± 0.15 v 1.81 ± 0.09 nmol/mL, P < .001). These data confirm that in end-stage renal failure, an increased oxidative stress is present and is able to induce protein damage. After transplantation, the CG content in protein was reduced (1.34 ± 0.08 nmol/mg protein), but it was not significantly different from the level in the HD group. The failure to return to the normal range suggests that an impaired redox status is maintained, resulting in a sustained elevation of CG. Conversely, the level of TBARS in transplanted patients (1.99 ± 0.22 nmol/mL) was not significantly different from that in the control group (1.81 ± 0.09), suggesting that lipoperoxidation may be inhibited. These results may be explained by the different turnover rates of the molecules and by the distinct origin of the two markers, resulting from the damage of proteins or lipids. Thus, lipoperoxidation would produce rapidly removable molecules, whereas protein oxidation damage would tend to accumulate. However, the significant correlation found between CGs and TBARS indicates that a common cause (oxidative stress) binds the two markers of damage.

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 Supported in part by Ministero dell'Università e della Ricerca Scientifica e Technologica (MURST) (60%) and Consiglio Nazionale delle Richerche (CNR) Grants No. 93.02041.CT14 and 94.00297.CT14.

PII: S0026-0495(96)90108-0

Metabolism - Clinical and Experimental
Volume 45, Issue 11 , Pages 1319-1322, November 1996