title: Paraoxonase and superoxide dismutase gene polymorphisms and noise-induced hearing loss.
abstract: BACKGROUND
  Noise-induced cochlear epithelium damage can cause hearing loss in industrial workers. In experimental systems, noise induces the release of free radicals and may damage the cochlear sensorial epithelium. Therefore, genes involved in regulating the reactive oxygen species manganese-superoxide dismutase (SOD2) and the antioxidant paraoxonase (PON) could influence cochlea vulnerability to noise. We evaluated whether susceptibility to noise-induced hearing loss (NIHL) is associated with SOD2, PON1, and PON2 polymorphisms in workers exposed to prolonged loud noise.
  
  
  METHODS
  We enrolled 94 male workers from an aircraft factory in the study. The SOD2 gene was screened by denaturing reversed-phase HPLC, and the PON1 (Q192R and M55L) and PON2 (S311C) polymorphisms were analyzed by PCR amplification followed by digestion with restriction endonucleases.
  
  
  RESULTS
  Three known (A16V, IVS3-23T/G, and IVS3-60T/G) and two new SOD2 polymorphisms (IVS1+ 8A/G and IVS3+107T/A) were identified. Regression analysis showed that PON2 (SC+CC) [odds ratio (OR) = 5.01; 95% confidence interval (CI), 1.11-22.54], SOD2 IVS3-23T/G and IVS3-60T/G (OR = 5.09; 95% CI, 1.27-20.47), age (OR = 1.22; 95% CI, 1.09-1.36), and smoking (OR = 49.49; 95% CI, 5.09-480.66) were associated with NIHL. No association was detected for PON1 (QQ+RR) and PON1 (LL) genotypes.
  
  
  CONCLUSIONS
  Our data suggest that SOD2 and PON2 polymorphisms, by exerting variable local tissue antioxidant roles, could predispose to NIHL. However, caution should be exercised in interpreting these data given the small sample size and the difficulty in matching cases to controls regarding the overwhelming risk factor, i.e., smoking at least 10 cigarettes/day.
authors.affiliation: Dipartimento di Biochimica e Biotecnologie Mediche, Università di Napoli Federico II and CEINGE scarl, Napoli, Italy.
authors.forename: Giuliana
authors.initials: G
authors.lastname: Fortunato
authors.forename: Elio
authors.initials: E
authors.lastname: Marciano
authors.forename: Federica
authors.initials: F
authors.lastname: Zarrilli
authors.forename: Cristina
authors.initials: C
authors.lastname: Mazzaccara
authors.forename: Mariano
authors.initials: M
authors.lastname: Intrieri
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Calcagno
authors.forename: Dino F
authors.initials: DF
authors.lastname: Vitale
authors.forename: Paolo
authors.initials: P
authors.lastname: La Manna
authors.forename: Claudio
authors.initials: C
authors.lastname: Saulino
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Marcelli
authors.forename: Lucia
authors.initials: L
authors.lastname: Sacchetti
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000378:metabolism; D043303:Aryldialkylphosphatase / Q000235:genetics*; D001301:Audiometry, Pure-Tone; D002851:Chromatography, High Pressure Liquid; D005609:Free Radicals / Q000097:blood; D020022:Genetic Predisposition to Disease; D006317:Hearing Loss, Noise-Induced / Q000175:diagnosis / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009784:Occupational Diseases / Q000175:diagnosis / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012044:Regression Analysis; D012307:Risk Factors; D013482:Superoxide Dismutase / Q000235:genetics*; D000099156:Superoxide Dismutase 2
chemical_list: D000975:Antioxidants; D043303:Aryldialkylphosphatase; D005609:Free Radicals; D013482:Superoxide Dismutase; D000099156:Superoxide Dismutase 2; C468406:PON1 protein, human; C468411:PON2 protein, human