title: Polymorphisms in genes involved in oxidative stress response in patients with sudden sensorineural hearing loss and Ménière's disease in a Japanese population.
abstract: The etiologies of idiopathic sudden sensorineural hearing loss (SSNHL) and Ménière's disease remain unclear. Recently, accumulating evidence has demonstrated that oxidative stress is related to the pathology of inner ear disease. Because genetic factors may contribute partly to the etiologies of SSNHL and Ménière's disease, we investigated the associations between genetic polymorphisms located in oxidative stress response genes and susceptibility to SSNHL and Ménière's disease. We compared 84 patients affected by SSNHL, 82 patients affected by Ménière's disease, and 2107 adults (1056 men and 1051 women; mean age, 59.2 years; range, 40-79 years) who participated in the National Institute for Longevity Sciences, Longitudinal Study of Aging. Multiple logistic regression was used to calculate odds ratios for SSNHL and Ménière's disease in individuals with polymorphisms in the genes glutathione peroxidase 1 (GPX1) (Pro198Leu, rs1050450), paraoxonase 1 (PON1) (Gln192Arg, rs662; and Met55Leu, rs854560), PON2 (Ser311Cys, rs7493), and superoxide dismutase 2 (SOD2) (Val16Ala, rs4880), with adjustment for age and gender. No significant differences in the distribution of the genotypes at these polymorphisms were observed among individuals with SSNHL and Ménière's disease and controls. No significant risk for SSNHL and Ménière's disease was observed in the additive genetic model, regardless of moderating variables. The C allele of SOD2 (rs4880) was more frequent in Ménière's disease cases with a hearing level over 50 dB compared with cases with a hearing level below 50 dB, suggesting that this polymorphism is associated with progression of a hearing loss in Ménière's disease. In conclusion, no significant associations between the polymorphisms of GPX1, PON1, PON2, and SOD2 and risk of SSNHL and Ménière's disease were observed in this Japanese case-control study.
authors.affiliation: Department of Otorhinolaryngology, Nagoya University Graduate School of Medicine, Nagoya, Japan. masaaki@med.nagoya-u.ac.jp
authors.forename: Masaaki
authors.initials: M
authors.lastname: Teranishi
authors.forename: Yasue
authors.initials: Y
authors.lastname: Uchida
authors.forename: Naoki
authors.initials: N
authors.lastname: Nishio
authors.forename: Ken
authors.initials: K
authors.lastname: Kato
authors.forename: Hironao
authors.initials: H
authors.lastname: Otake
authors.forename: Tadao
authors.initials: T
authors.lastname: Yoshida
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Suzuki
authors.forename: Michihiko
authors.initials: M
authors.lastname: Sone
authors.forename: Saiko
authors.initials: S
authors.lastname: Sugiura
authors.forename: Fujiko
authors.initials: F
authors.lastname: Ando
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Shimokata
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Nakashima
mesh_terms: D000328:Adult; D000368:Aged; D043303:Aryldialkylphosphatase / Q000235:genetics; D044466:Asian People / Q000235:genetics*; D016022:Case-Control Studies; D005260:Female; D005787:Gene Frequency; D005979:Glutathione Peroxidase / Q000235:genetics; D006319:Hearing Loss, Sensorineural / Q000235:genetics*; D003639:Hearing Loss, Sudden / Q000235:genetics*; D006801:Humans; D008297:Male; D008575:Meniere Disease / Q000235:genetics*; D008875:Middle Aged; D018384:Oxidative Stress / Q000235:genetics*; D011110:Polymorphism, Genetic; D013482:Superoxide Dismutase / Q000235:genetics; D000094765:Glutathione Peroxidase GPX1; D000099156:Superoxide Dismutase 2
chemical_list: D043303:Aryldialkylphosphatase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D000094765:Glutathione Peroxidase GPX1; D000099156:Superoxide Dismutase 2; C468406:PON1 protein, human; C468411:PON2 protein, human; C000722067:GPX1 protein, human