| Generally, hearing loss is associated with environmental and genetic factors. For noise-induced hearing loss(NIHL), mostly believe that noise environment is the mainly etiological factor, we consider that there are obviously individual variations the same as aminoglycoside antibiotics induced deafness (AAID) through several times investigation and a lot of related research. Recent findings indicate that a large proportion of both syndromic and nonsyndromic forms of deafness are caused by a small number of genes. This study focused on epidemiology and predisposing genes of NIHL, furthermore, provid the evidence to the gene diagnosis and treatment.In this study, through health examination, whole of the data and one hundred and eighty two blood samples were collected from 344 soldiers who exposed to military noise in Beijing, including susceptible and tolerance groups. Genomic DNA was isolated, and then the targeted fragments of mitochondrial DNA and coding region of GJB2 gene were amplified by polymerase chain reaction (PCR). The PCR products were analyzed by direct sequencing. There were 98 mtDNA variants (41 reside in 12SrRNA) and 12 GJB2 gene variants; among them, mtDNA T1095C and G7642A coexisted in 4 susceptible individuals, but these mutations were not found in tolerant group. In addition, 3 tolerant individuals carry 961delT+insC and meanwhile individuals in susceptible group don't have; heterozygous GJB2 235delC mutation was found 2 in susceptible group and 1 in tolerant group respectively; one G7444A and one homozygous G109A were found only in susceptible group.The results revealed: The influence of noise exposure on hearing is significant and the hearing loss has individual differences. The 12SrRNA is an area with high variant and mutation rate. The coexistence of mtDNA T1095C and G7642A in susceptible group exposed to the similar noise environment suggests these mutations are pathogenic mutations associated with NIHL. Three tolerant individuals with history of long-term exposure to noise environment carry 961delT+insC and this result suggests 961delT+insC might be a conditional pathogenic mutation but not correlate with NIHL. |