Investigating the Effects of Exposure to Continuous White Noise on SLC26A4 Gene Expression Levels in Male Rat Cochlea

Background and purpose: Irreversible damage to the inner ear is known as noise-induced hearing loss (NIHL). Exposure to excessive noise can affect the expression of genes in molecules involved in development of NIHL. SLC26A4 gene or PDS is responsible for causing both syndromic and non-syndromic deafness and is located at DFNB site. The aim of this study was to investigate the expression level of this gene due to continuous white noise exposure. Materials and methods: In this experimental study, 10 healthy male Wistar rats were divided into exposure group (n=6) and control group (n=4). Exposur group was exposed to continuous white noise (8hr/day, 6days, SPL=110±5dB) in noise chambers. Cochlear biopsy was done 1 hour (n=5) and 1 week (n=5) after exposure and then, RNA extraction, cDNA synthesis and Real-Time PCR analysis were done. In addition, histological analyzes were performed. Data analysis was done using One-Way ANOVA (95% CI diff.). Results: At both 1 hour and 1 week after exposure, the expression of SLC26A4 gene decreased significantly (P= 0.0005 and P= 0.0003, respectively). The fold changes compared to the control group (=1) were 0.0733 and 0.00712, respectively. Histological images illustrated serious damage to the cochlea. Conclusion: Sensorineural deafness will happen if exposure to intense noise continues and subsequently down-regulation of SLC26A4 in the cochlea occur during longer discontinuation and in case of expression level failure to return to its basal level

اثرات صدای بنفش بر روی میزان بیان ژن SLC26A4در بافت حلزون گوش رت

Background and Aims: As one of the most important physical detrimental factors, purple noise can be considered similar to sounds that a wide range of people are exposed to in their workplaces. Also, cochlear tissue samples are the best tissue samples to evaluate gene expression and pathologic studies following noise exposure. Therefore, the aim of this study was to investigate the effects of purple noise on the expression of SLC26A4 gene in cochlear tissue. Methods & material: Totally, 10 male Wistar rats were used in this experimental study. Both N1 and N2 exposure groups were exposed to purple noise with sound pressure level of 115-120 dB and frequency range of 4-20 kHz. Histological tests were performed for pathological studies. Finally, the relative expression of SLC26A4 gene was determined by qRT-PCR technique. All experiments were conducted according to ethical standards of working with laboratory animals. Results: The results showed that the expression of SLC26A4 gene decreased significantly compared to the normal level in both N1 and N2 groups. The results of cochlear tissue pathology showed that the group exposed to purple noise for 6 days had more mechanical damage 7 days after cessation of exposure. Conclusion: Significant decreased expression in SLC26A4 gene and permanent damage to the Reissner and Basal lamina membranes in the cochlear tissue and the auditory nerve ganglion leads to strengthening the incidence of advancing sensorineural hearing impairment and increases the likelihood of metastasis in cochlear tissue.زمینه و اهداف: صدای بنفش را می­توان مشابه اصواتی در نظر گرفت که طیف وسیعی از افراد به عنوان یکی از مهم­ترین عوامل فیزیکی زیان­ آور، در محیط­های کاری خود در تماس با آن هستند. از طرفی، نمونه­ی بافت حلزون گوش بهترین نمونه بافتی جهت بررسی میزان بیان ژن­ و مطالعات آسیب شناسی، پس از تماس با اصوات محسوب می­شوند لذا هدف از این پژوهش، بررسی اثرات صدای بنفش بر روی میزان بیان ژن  SLC26A4در بافت حلزون گوش بود.   مواد و روش­ها: در مجموع، 10 سر رت نر با نژاد ویستار در این مطالعه تجربی استفاده گردید. دو گروه مواجههN1  و N2 در تماس با صدای بنفش (kHz20-4، dB120-115=SPL) قرار گرفتند. آزمایشات بافت شناسی جهت مطالعات آسیب شناسی بافت صورت گرفت و در پایان، میزان بیان نسبی ژن SLC26A4 بوسیله ی qRT-PCR تعیین گردید. کلیه آزمایشات این مطالعه، طبق موازین اخلاقی کار با حیوانات آزمایشگاهی انجام گرفت.   یافته ها: نتایج نشان داد که در هر دو گروه مواجهه N1 و N2 کاهش معنادار میزان بیان ژن SLC26A4 نسبت به سطح نرمال اتفاق افتاده است. نتایج مطالعه­ی آسیب­ شناسی بافت حلزون گوش نشان داد که نمونه ی گروهی که 6 روز با صدای بنفش مواجهه داشت، پس از 7روز از قطع مواجهه صدمات مکانیکی بیشتری دیده بود.   نتیجه­گیری: این سطح از کاهش بیان در ژن SLC26A4 و آسیب دائمی غشای رایسنر و بازال لامینا در بافت حلزون گوش و گانگلیون عصب شنوایی، منجر به تقویت بروز نقص شنوایی حسی-عصبی پیش رونده و افزایش احتمال متاستاز در بافت حلزون گوش می­گردد