تأثیر آلودگی صوتی در انتشار گلیکوکانژوگه‌های سطح سلول در گانگلیون مارپیچی نوزاد موش

Authors

  •  زهرا وجدانی,
  •  فرزانه دهقانی,
  •  محمد رضا عرب,
  •  ملیحه منصفی,
  • طاهره طلایی خوزانی,
Abstract:

Background: Some pregnant women are exposed to occupational noise, a risk factor for the development of the auditory system. The auditory system is one of the areas in embryonic development in which noise might induce aberrant development. Noise can change the gene expression pattern of an embryo and thereby modify the physiology of the auditory system. Therefore, noise can change the molecular structure of the developing ear. One of the critical molecules involved in development of auditory system is glycoconjugate. The aim of this study was to investigate the molecular changes of the developing spiral ganglion after exposure to industrial levels of noise.Methods: A total of 42 pregnant mice were divided into control and experimental groups. Each group was further divided into three subgroups. The three experimental subgroups were exposed to daily noise with an intensity of 100 db for 2.5 hours until sacrifice (for the first group to be sacrificed) or day seven of postnatal life (for the other two groups). The mice offspring were sacrificed at the first, seventh and 14th days of postnatal life. The inner ears were prepared histologically. The specimens were stained with the lectins wheat germ antigen (WGA), peanut agglutinin (PNA), Dolichos biflorus agglutinin (DBA) and BSAI-B4. Results: The results indicated that, although there were no histological changes at the light-microscopic level in the ear development, statistical analysis showed that there was a significant decrease in the uptake of the BSA1-B4 lectin by neurons of spiral ganglion in 14th day of postnatal life in the experimental group compared to  that of the control group (p<0.05). Conclusions: After noise exposure, in spite of normal neuronal structure, these cells were modified at the molecular level, especially in glycoconjugate expression, influencing the normal physiology of neurons and causing auditory disorders.

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volume 65  issue None

pages  1- 6

publication date 2007-09

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