N-Acetylcysteine (NAC) is used intravenously (i.v.) at high doses for the prevention
of acute kidney injury after cardiac surgery [
[1]
] and in contrast-induced nephropathy (CIN) [
[2]
]. Although the underlying mechanisms are not yet fully understood, altered nitric
oxide (NO) and prostaglandin (PG) synthesis and elevated oxidative stress are assumed
to play a crucial role, and NAC is currently considered as one of the best choices
to prevent CIN in high-risk groups [
[2]
]. Yet, a systematic meta-analysis of randomized controlled trials showed that prophylactic
perioperative NAC in cardiac surgery does not reduce acute renal injury, haemodialysis,
or death [
[3]
]. We reasoned that NAC and its derivatives cysteine (Cys) and glutathione (GSH) may
exert effects primarily not related to their intrinsic antioxidant activity. The aim
of the present work was to investigate the acute effects of NAC in patients undergoing
cardiac surgery and in healthy subjects on NO, PGE2, and oxidative stress. These studies are described in detail below. Whole body NO
synthesis was estimated by measuring the urinary excretion of the NO metabolites nitrite
and nitrate [
[4]
]. Renal synthesis of the cyclooxygenase (COX)-dependent PGE2 was measured by analysing PGE2 in urine [
[5]
]. Whole body oxidative stress was assessed by measuring the F2-isoprostane 15(S)-8-iso-PGF2α in urine samples [
[6]
]. Urinary excretion of these biomarkers was corrected for urinary creatinine excretion.Keywords
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Article info
Publication history
Published online: September 27, 2014
Accepted:
September 20,
2014
Received:
September 8,
2014
Identification
Copyright
© 2014 Elsevier Ireland Ltd. Published by Elsevier Inc. All rights reserved.