Higher levels of antioxidant defenses in enalapril-treated versus non-enalapril-treated hemodialysis patients.
We previously reported chronic treatment with angiotensin-converting enzyme inhibitors (ACEis) increases antioxidant defenses in mice. In the present study, however, we examined various antioxidant defenses in chronic hemodialysis (HD) patients either treated with enalapril (10 mg/d) for at least 6 months (+ACEi; n = 11) or untreated (-ACEi; n = 11). The relationship between antioxidant status and HD was investigated by determining oxidative stress markers and antioxidant defenses in a group of chronic HD patients (n = 33) and a group of age-matched controls (n = 29). The effect of a single HD session on those parameters was also evaluated. Before an HD session (pre-HD), HD patients had significantly lower levels of red blood cell (RBC) glutathione (GSH), selenium-dependent glutathione peroxidase activity (RBC-Se-GPx), plasma ubiquinol-10, and alpha-tocopherol than controls. In a randomly selected group of patients (n = 19), a single HD session caused an additional decrease in RBC-GSH and plasma ubiquinol-10 levels. Plasma thiobarbituric acid reactive substance (TBARS) levels were significantly greater in pre-HD patients than controls. Post-HD plasma TBARS levels were similar to control values. The cohort of +ACEi HD patients had greater pre-HD RBC-GSH content, RBC-Se-GPx activity, and plasma beta-carotene concentrations than -ACEi patients (RBC-GSH: +ACEi, 3.1 +/- 0.9 micromol/mL packed RBCs [PRBCs]; -ACEi, 1.2 +/- 0.3 micromol/mL PRBCs [P < 0.05 v +ACEi]; RBC-Se-GPx: +ACEi, 5.8 +/- 0.7 U/mL PRBCs; -ACEi, 4.3 +/- 0.2 U/mL PRBCs [P < 0.05 v +ACEi]; plasma beta-carotene: +ACEi, 0.54 +/- 0.16 micromol/L plasma; -ACEi, 0.19 +/- 0.05 micromol/L plasma [P < 0.05 v +ACEi]). Results show profound alterations in the circulating antioxidant systems of chronic HD patients and that additional oxidative stress occurs during the HD procedure. In addition, in +ACEi HD patients, the levels of several antioxidant defenses are greater than in those in -ACEi HD patients.
de Cavanagh
E M
EM
Department of Experimental Nephrology, School of Pharmacy and Biochemistry, Buenos Aires, Argentina.
Ferder
L
L
Carrasquedo
F
F
Scrivo
D
D
Wassermann
A
A
Fraga
C G
CG
Inserra
F
F
D000328:Adult; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage* / Q000009:adverse effects; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000097:blood; D004656:Enalapril / Q000008:administration & dosage* / Q000009:adverse effects; D004912:Erythrocytes / Q000201:enzymology; D005260:Female; D005609:Free Radicals; D005978:Glutathione / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D006801:Humans; D007676:Kidney Failure, Chronic / Q000201:enzymology / Q000628:therapy*; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D051379:Mice; D008875:Middle Aged; D017382:Reactive Oxygen Species / Q000378:metabolism; D006435:Renal Dialysis; D014451:Ubiquinone / Q000031:analogs & derivatives / Q000097:blood; D014810:Vitamin E / Q000097:blood
D000806:Angiotensin-Converting Enzyme Inhibitors; D000975:Antioxidants; D005609:Free Radicals; D017382:Reactive Oxygen Species; D014451:Ubiquinone; D014810:Vitamin E; D008315:Malondialdehyde; C026663:ubiquinol-10; D004656:Enalapril; D002374:Catalase; D005979:Glutathione Peroxidase; D005978:Glutathione