Thromb Haemost 2017; 117(12): 2334-2345
DOI: 10.1160/TH17-05-0356
Blood Cells, Inflammation and Infection
Schattauer GmbH Stuttgart

Erythrocyte Membrane Fluidity Alterations in Sudden Sensorineural Hearing Loss Patients: The Role of Oxidative Stress

Matteo Becatti
,
Rossella Marcucci
,
Amanda Mannucci
,
Anna Maria Gori
,
Betti Giusti
,
Francesco Sofi
,
Lucia Mannini
,
Anna Paola Cellai
,
Agatina Alessandrello Liotta
,
Marco Mugnaini
,
Giacomo Emmi
,
Domenico Prisco
,
Niccolò Taddei
,
Claudia Fiorillo
Further Information

Publication History

24 May 2017

16 August 2017

Publication Date:
06 December 2017 (online)

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Abstract

Introduction Sudden sensorineural hearing loss (SSNHL) involves an acute unexplained hearing loss, nearly always unilateral, that occurs over less than a 72-hour period. SSNHL pathogenesis is not yet fully understood. Cochlear vascular occlusion has been proposed as a potential mechanism of hearing damage and cochlear ischaemia has been related to alterations of cochlear microvessels. In addition, some researchers have focused their attention on the rheological alterations and blood hyperviscosity. Erythrocyte deformability plays a key role in determining blood viscosity, and it is critical to cochlear perfusion. It has been shown that oxidative stress-induced erythrocyte membrane fluidity alterations are linked to the progression of cardiovascular diseases.

Methods To determine whether erythrocytes from SSNHL patients show signs of oxidative stress, and whether this condition can modify the haemorheologic profile in these patients, we analysed haemorheologic profile and erythrocyte oxidative stress in 35 SSNHL patients and 35 healthy subjects, matched for age and sex. Fluorescence anisotropy was used to evaluate the fluidity of erythrocyte membranes.

Results Our results show a significant structural and functional involvement of erythrocyte membrane alterations in SSNHL, as well as elevated levels of membrane lipid peroxidation and intracellular reactive oxygen species (ROS) production. In addition, erythrocyte-derived ROS and erythrocyte lipid peroxidation positively correlated with whole blood viscosity and erythrocyte deformability. Moreover, in vitro experiments demonstrated that ROS display a key role in erythrocyte membrane fluidity.

Conclusion These findings indicate that erythrocyte oxidative stress plays a key role in the pathogenesis of SSNHL and pave the way to new therapeutic interventions.

Acknowledgment

This study was supported by “Fondi di Ateneo” research funding from the University of Florence to Claudia Fiorillo.