A comprehensive study of oxidative stress in sudden hearing loss.


Gul F. , Muderris T., Yalciner G., Sevil E., Bercin S. , Ergin M., et al.

European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery, cilt.274, ss.1301-1308, 2017 (SCI Expanded İndekslerine Giren Dergi) identifier identifier

  • Cilt numarası: 274 Konu: 3
  • Basım Tarihi: 2017
  • Doi Numarası: 10.1007/s00405-016-4301-1
  • Dergi Adı: European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • Sayfa Sayısı: ss.1301-1308

Özet

Little is known about the association between idiopathic sudden sensorineural hearing loss (ISSNHL) and oxidative stress. We investigated changes in a wide range of oxidants and antioxidants to create a comprehensive picture of oxidative imbalance. In the peripheral blood of 50 ISSNHL patients and 50 healthy subjects, total oxidant status (TOS), total antioxidant status (TAS), paraoxonase (PON), thiol/disulphide levels were measured. Moreover, a global oxidative stress index, reflecting both oxidative and antioxidant counterparts, was also calculated. One-way analysis between oxidative markers and severity of hearing loss were evaluated. The ISSNHL patients showed significantly higher TOS levels than controls (6.02 +/- 3.17 vs. 4.5 +/- 2.22; p = 0.018). The oxidative index was also significantly higher in patients than controls (0.39 +/- 0.19 vs. 0.3 +/- 0.14; p = 0.035). TAS, PON, native thiol, and total thiol were not altered. There was no statistical significance between oxidative markers and severity of hearing loss. The binary logistic regression model revealed that disulphide and TOS were associated with ISSNHL. There are alterations in a wide array of oxidants and antioxidants, with balance shifting toward increased oxidative stress in ISSNHL. Our findings may suggest endothelial dysfunction in ISSNHL etiopathogenesis.