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Clinical Chemistry 50: 2012-2018, 2004. First published September 2, 2004; 10.1373/clinchem.2004.037788
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(Clinical Chemistry. 2004;50:2012-2018.)
© 2004 American Association for Clinical Chemistry, Inc.


Molecular Diagnostics and Genetics

Paraoxonase and Superoxide Dismutase Gene Polymorphisms and Noise-Induced Hearing Loss

Giuliana Fortunato1, Elio Marciano2, Federica Zarrilli3, Cristina Mazzaccara1, Mariano Intrieri1,3, Giuseppe Calcagno1, Dino F. Vitale4, Paolo La Manna5, Claudio Saulino2, Vincenzo Marcelli2 and Lucia Sacchetti1,a

1 Dipartimento di Biochimica e Biotecnologie Mediche, Università di Napoli Federico II and CEINGE scarl, Napoli, Italy.
2 Dipartimento di Neuroscienze e Scienze del Comportamento, Università di Napoli Federico II, Napoli, Italy.
3 Dipartimento di Scienze e Tecnologie per l’Ambiente e il Territorio, Facoltà di Scienze MM FF NN, Università del Molise, Isernia, Italy.
4 Fondazione Salvatore Maugeri, IRCCS Istituto di Campoli Telese, Benevento, Italy.
5 Alenia Aereonautica, Stabilimento Pomigliano D’Arco, Napoli, Italy.

aAddress correspondence to this author at: Dipartimento di Biochimica e Biotecnologie Mediche, Università di Napoli Federico II and CEINGE scarl, via S. Pansini 5, 80131 Napoli, Italy. Fax 39-081-7462404; e-mail sacchetti{at}dbbm.unina.it.

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.




The following articles in journals at HighWire Press have cited this article:


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Arterioscler. Thromb. Vasc. Bio.Home page
G. Fortunato, M. D. Di Taranto, U. M. Bracale, L. Del Guercio, F. Carbone, C. Mazzaccara, A. Morgante, F. P. D'Armiento, M. D'Armiento, M. Porcellini, et al.
Decreased Paraoxonase-2 Expression in Human Carotids During the Progression of Atherosclerosis
Arterioscler. Thromb. Vasc. Biol., March 1, 2008; 28(3): 594 - 600.
[Abstract] [Full Text] [PDF]




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