Oxidative stress, nitric oxide, endothelial dysfunction and tinnitus.

Area of Science:

• Neurology
• Vascular Biology
• Otolaryngology

Background:

• Acute idiopathic tinnitus is a complex condition with unclear pathophysiology.
• Endothelial dysfunction is implicated in various vascular disorders.

Purpose of the Study:

• To investigate the role of pathogenic endothelial dysfunction in acute idiopathic tinnitus.
• To analyze specific biomarkers of oxidative stress and endothelial function in tinnitus patients.

Main Methods:

• Blood samples were collected from the internal jugular and brachial veins of 44 tinnitus patients and 25 healthy volunteers.
• Assessed levels of malonaldehyde, 4-hydroxynonenal, myeloperoxidase, glutathione peroxidase, nitric oxide, L-arginine, L-ornitine, thrombomodulin (TM), and von Willebrand factor (vWF) activity.
• Compared biomarker levels during tinnitus and asymptomatic periods, and between jugular and brachial circulation.

Main Results:

• Patients with tinnitus showed higher jugular blood concentrations of oxidative markers and L-arginine.
• Lower nitric oxide and L-ornitine levels were observed in the jugular blood of tinnitus patients.
• Significantly elevated TM and vWF activity were found in the jugular blood of patients compared to brachial blood.

Conclusions:

• Acute tinnitus is associated with increased oxidant production, TM, and vWF activity in cerebral circulation.
• Reduced nitric oxide production in brain circulation contributes to tinnitus pathophysiology.
• These findings suggest cerebro-vascular endothelial dysfunction leading to inner ear microcirculation impairment in tinnitus.