Antioxidant status and hearing function in noise-exposed workers

Rabinowitz, Peter; Wise, John Pierce; Mobo, Ben Hur; Antonucci, Peter G; Powell, Carol A.; Slade, Martin D.

doi:10.1016/s0378-5955(02)00350-7

Cited by 81 publications

(76 citation statements)

References 24 publications

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“…However, firm evidence for the involvement of genetic factors in human NIHL is still scarce. A possible association between the absence of glutathione-S-transferase M1 (GSTM1) and NIHL was reported (Rabinowitz et al 2002), but this was not confirmed in a recent study on 2 deletion polymorphisms in the GSTM1 and GSTT1 genes and the susceptibility to NIHL using susceptible and resistant NIHL in a Caucasian population from 3 distinct workplaces (Carlsson et al 2005). Another study suggested that SOD2 and paraoxonase polymorphisms could predispose to NIHL (Fortunato et al 2004) The HSP70 family proteins may be the most predominant and particularly interesting group of proteins involved in the major histocompatibility complex in disease susceptibility (Favatier et al 1997).…”

Section: Discussionmentioning

confidence: 99%

Association of hsp70 polymorphisms with risk of noise-induced hearing loss in Chinese automobile workers

Yang¹,

Tan²,

Yang³

et al. 2006

Cell Stress Chaper

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Severe noise exposure can induce heat shock proteins (Hsps), and exposure to moderate noise has been reported to confer protection against noise-induced damage to hearing. Whether there is any association of genetic variation in both constitutive and inducible hsp70 genes with noise-induced hearing loss (NIHL) is presently unknown. Using polymerase chain reaction-restriction fragment length polymorphism, we genotyped 3 polymorphisms (ϩ190A/ B, ϩ1267A/B, and ϩ2437A/B) in the hsp70-1 (rs1043618), hsp70-2 (rs1061581), and hsp70-hom (rs2227956) genes, respectively, and investigated the associations of these polymorphisms with risk of developing NIHL in 194 automobile workers working in a similar noise environment as evaluated by audiological assessment. Multivariate logistic regression models were used to assess the associations with the risk genotypes, and Whap software was used to analyze their haplotypes. Our results showed that there was no statistically significant difference in the genotype and allele distributions of hsp70-1, hsp70-2, and hsp70-hom between the NIHL group and the normal group (P Ͼ 0.05) with and without adjustment for age, sex, smoking, history of explosive noise exposure, and cumulative noise exposure. However, haplotype analysis revealed that the Hap5 (ie, haplotype ϩ190A/ϩ1267B/ϩ2437A) and Hap6 (ie, haplotype ϩ190A/ϩ1267B/ϩ2437B) were significantly more frequent in the NIHL group than in the normal group (20/9, P ϭ 0.022, and 7/0, P ϭ 0.005, respectively). Compared with Hap1 (ie, ϩ190A/ϩ1267A/ϩ2437A), Hap5 was associated with a nearly 3-fold increased risk of NIHL (adjusted odds ratio, 2.67; 95% confidence interval, 1.13-6.27). Seven of the NIHL patients had Hap6, but none of the controls had this haplotype. Our results suggest that some haplotypes of the hsp70 genes may be associated with a higher susceptibility to NIHL.

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Section: Discussionmentioning

confidence: 99%

Association of hsp70 polymorphisms with risk of noise-induced hearing loss in Chinese automobile workers

Yang¹,

Tan²,

Yang³

et al. 2006

Cell Stress Chaper

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“…That antioxidant agents effectively reduce sensory cell death and NIHL has now been well demonstrated in animal studies using a variety of antioxidant agents, such as GSH/ glutathione monoethyl ester (GSHE) (Ohinata et al, 2000b;Kopke et al, 2002;Hight et al, 2003;Miller et al, 2003a), resveratrol (Seidman et al, 2003), allopurinol (Seidman et al, 1993;Cassandro et al, 2003), superoxide dismutase-polyethylene glycol (Seidman et al, 1993), U74389F (a lazaroid drug which inhibits lipid peroxidation and scavenges free radicals) (Quirk et al, 1994), and R-phenylisopropyladenosine (R-PIA) (Hu et al, 1997;Hight et al, 2003). Small protective effects of individual (or combined) dietary antioxidant nutrients are also well described for insults to the inner ear including noise, drugs, and age (Chole and Quick, 1976;Lohle, 1980Lohle, ,1985Romeo, 1985;Biesalski et al, 1990;Lopez-Gonzalez et al, 2000;Seidman, 2000;Bertolaso et al, 2001;Pasqualetti and Rijli, 2001;Teranishi et al, 2001;Rabinowitz et al, 2002;Hou et al, 2003;Derekoy et al, 2004;Kalkanis et al, 2004;Weijl et al, 2004;Ahn et al, 2005;McFadden et al, 2005;Yamashita et al, 2005a).…”

Section: Enhancing Antioxidant Defense Attenuates Nihlmentioning

confidence: 99%

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

et al. 2007

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Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7-10 days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3 days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss.

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“…These null genotypes cannot conjugate metabolites specific for these enzymes, rendering these individuals more prone to damage caused by oxidative stress and possibly more susceptible to ARHL. GSTM1-null individuals have been shown to have lower amplitudes of high frequency otoacoustic emissions compared to individuals possessing the gene, indicating that GSTM1-null individuals might be more prone to ARHL [57]. The enzyme of Nacetylation (NAT) is also known to be involved in mediation of xenobiotic toxicity.…”

Section: Oxidative Stressmentioning

confidence: 99%

Ageing and hearing loss

Yan

2007

The Journal of Pathology

278

178

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Although many adults retain good hearing as they age, hearing loss associated with ageing is common among elderly persons. There are a number of pathophysiolological processes underlying age-related changes to functional components in the inner ear. Genetic factors determine the ageing process but are under the influence of intrinsic and environmental factors. It is difficult to distinguish changes of normal ageing from those of other contributing factors. The effects of age-related deafness can have significant physical, functional and mental health consequences. Although a deficit in hearing can be corrected to some degree by a hearing aid or other appropriate amplification devices, hearing-related rehabilitative needs are much more than simply amplifying external sound. Only by better understanding the process of ageing and its effect on the auditory function can we better accommodate elderly people in our day-to-day interactions. We review here the structure and function of the inner ear, pathophysiology associated with age-related hearing loss (ARHL), heritability, allelism and modifier genes of ARHL, and evaluate the genetic analyses for identification of genetic factors that are involved.

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Antioxidant status and hearing function in noise-exposed workers

Cited by 81 publications

References 24 publications

Association of hsp70 polymorphisms with risk of noise-induced hearing loss in Chinese automobile workers

Association of hsp70 polymorphisms with risk of noise-induced hearing loss in Chinese automobile workers

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

Ageing and hearing loss

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