Impairment of serum albumin antioxidant properties in obstructive sleep apnoea syndrome

¹ HP2 Laboratory (Hypoxia: Pathophysiology) INSERM ERI 17, EA 3745 Joseph Fourier University, Grenoble, France; and DBI, University Hospital Grenoble, France
² Sleep Laboratory, EFCR University Hospital Grenoble, France; and HP2 Laboratory (Hypoxia: Pathophysiology) INSERM ERI 17, EA 3745 Joseph Fourier University, Grenoble, France
³ Dept of Cardiology and Hypertension, University Hospital, Grenoble, France
⁴ DBI, University Hospital Grenoble, France
⁵ Endocrinologie, Diabétologie Nutrition DigiDUNE, University Hospital Grenoble, France

^* To whom correspondence should be addressed. E-mail: JPepin{at}chu-grenoble.fr.

	Abstract

Antioxidant counteraction to oxidative stress has been poorly explored in obstructive sleep apnoea (OSA). Serum albumin is a major antioxidant agent and structural modifications induced by glucose or free radicals impair its antioxidant properties.

To compare antioxidant capacities and structural changes of albumin in non obese OSA and in healthy volunteers.

Albumin structural changes were studied by quenching of fluorescence in the presence of acrylamide. Albumin thiols and fructosamines reflecting respectively oxidization and glycation-induced changes of serum albumin were assessed. Albumin structural changes were demonstrated by a significant decrease in quenching of fluorescence in OSA patients. Oxidization resulting in a significant decrease in thiol groups (3.7±0.7 versus 2.3±0.4 micromol·g^-1 proteins) and glycation associated with a significant increase in fructosamines (226.6±27 versus 286±44.4micromol·l^-1) were found when comparing healthy volunteers to OSA. There was a significant relationship between both parameters and sleep apnoea severity. After CPAP intervention, albumin thiols groups were reassessed in 7/16 OSA and increased significantly from 2.25±0.39 to 2.79±0.31µmol·g^-1 prot, p<0.001.

OSA patients demonstrated a reduction in serum albumin antioxidant properties that may aggravate oxidative stress and thus contribute to cardiovascular and metabolic morbidities.

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