4.5 Article

Disulfide stress in carbon monoxide poisoning

Journal

CLINICAL BIOCHEMISTRY
Volume 49, Issue 16-17, Pages 1243-1247

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.clinbiochem.2016.07.019

Keywords

Carbon monoxide poisoning; Disulfide; Oxidative stress; Thiol; Thiol-disulfide homeostasis

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Objectives: Carbon monoxide (CO) remains the most common cause of lethal poisoning around the world. The purpose of this study was to investigate the homeostasis between thiol-disulfide couples and to evaluate oxidative status comprehensively in acute CO poisoning, using new parameters along with other well-known oxidant-antioxidant molecules. Design and methods: This case study consisted of 43 subjects who were diagnosed with carbon monoxide poisoning and 35 healthy individuals who were used as controls. Thiol-disulfide paired tests were examined in both groups using the method developed recently. Results: Patients with CO poisoning had significantly higher levels of serum disulfide than the control patients (20.7 +/- 5.03 versus 16.43 +/- 3.97, p = 0.001). Native thiol and total thiol levels were lower in the CO patient group than in the control group (p < 0.001, for each variable). The disulfide/native thiol ratios and disulfide/ total thiol ratios were significantly higher, while native thiol/total thiol ratios were significantly lower, in patients with acute CO poisoning than in the healthy controls (p < 0.001, for all ratios). The disulfide/native ratios were negatively correlated with both total antioxidant response and paraoxonase and arylesterase values and were positively correlated with total oxidant status and ceruloplasmin values (p < 0.05, for all correlations). Conclusions: Excessive disulfide levels and their related ratios were found in CO poisoning patients. In particular, the disulfide/ native thiol ratio was identified as an indicator for overall oxidative status. Among CO poisoning patients, the thiol-disulfide balance was found to be impaired. Therefore, the disruption of thiol-disulfide homeostasis might be involved in CO toxicity. (C) 2016 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.

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