Albumin Cys34 adducted by acrolein as a marker of oxidative stress in ischemia-reperfusion injury during hepatectomy. (2nd August 2016)

• Record Type: Journal Article
• Authors: Witort, Ewa; Capaccioli, Sergio; Becatti, Matteo; Fiorillo, Claudia; Batignani, Giacomo; Pavoni, Vittorio; Piccini, Matteo; Orioli, Marica; Carini, Marina; Aldini, Giancarlo; Lulli, Matteo
• Is Part Of: Free radical research. Volume 50:Number 8(2016:Aug.)
• Page Start: 831
• Page End: 839
• Publication Date: 2016-08-02
• Subjects: Hepatic resection -- mass spectrometry -- protein carbonyls -- reactive carbonyl species; Free radicals (Chemistry) -- Periodicals; Antioxidants -- Periodicals; Vitamin C -- Periodicals; Vitamin E -- Periodicals; 541.224
• DOI: 10.1080/10715762.2016.1179736
• Languages: English
• ISSNs: 1071-5762

Abstract

Abstract: The aim of this study was to measure and identify the reactive carbonyl species (RCSs) released in the blood of humans subjected to hepatic resection. Pre-anesthesia malondialdehyde (MDA) plasma content (0.36 ± 0.11 nmol/mg protein) remained almost unchanged immediately after anaesthesia, before clamping and at the 10th min after ischemia, while markedly increased (to 0.59 ± 0.07 nmol/mg; p < 0.01, Tukey's post test) at the 10th min of reperfusion. A similar trend was observed for the protein carbonyls (PCs), whose pre-anesthesia levels (0.17 ± 0.13 nmol/mg) did not significantly change during ischemia, while increased more than fourfold at the 10th min of reperfusion (0.75 ± 0.17 nmol/mg; p < 0.01, Tukey's post test). RCSs were then identified as covalent adducts to the albumin Cys34, which we previously found as the most reactive protein nucleophilic site in plasma. By using a mass spectrometry (MS) approach based on precursor ion scanning, we found that acrolein (ACR) is the main RCS adducted to albumin Cys34. In basal conditions, the adducted albumin was 0.6 ± 0.4% of the native form but it increased by almost fourfold at the 10th min of reperfusion (2.3 ± 0.7%; p < 0.01, t -test analysis). Since RCSs are damaging molecules, we propose that RCSs, and ACR in particular, are new targets for novel molecular treatments aimed at reducing the ischemia/reperfusion damage by the use of RCS sequestering agents.