ABSTRACT
OBJECTIVE: The objective of this study was to investigate the influence of Ginkgo Biloba in early treatment of noise induced hearing loss on expression of IL-6, IL-1 Beta, TNF-alfa, HSP-70, HSF-1 and COX-2 in the rat cochlea. METHODS: Thirty two female rats were randomly divided into four groups (Acoustic Trauma, Ginkgo Biloba, Acoustic Trauma+Ginkgo Biloba, Non Treatment). Auditory brainstem response (ABR) was applied in all the groups. At the end of the study, IL-1Beta, IL-6, TNF-alpha, HSP-70, HSF-1 and COX-2 were studied in cochlear tissue with ELISA and Western blot analysis. RESULTS: There were significant increases in ABR values measured at days 1 and 7 compared to baseline values in Group 3. IL-1 Beta, IL-6 and TNF-alpha values were significantly higher in Group 1 than in the other groups. Whereas HSP-70 and HSF-1 values were found to be significantly lower in Group 1 compared to those in Group 2 and Group 3. COX-2 of Group 1 was significantly higher than the other groups. CONCLUSION: Ginkgo Biloba is helpful in the treatment of noise induced hearing loss and exerts its effect by inhibiting expression of IL-1 Beta, IL-6, TNF-alpha and COX-2 and increasing HSP-70 and HSF-1 values in rat cochlea.
Subject(s)
Cochlea/drug effects , Cyclooxygenase 2/drug effects , Cytokines/drug effects , Evoked Potentials, Auditory, Brain Stem/drug effects , HSP70 Heat-Shock Proteins/drug effects , Heat Shock Transcription Factors/drug effects , Noise , Plant Extracts/pharmacology , Animals , Blotting, Western , Cochlea/metabolism , Cyclooxygenase 2/metabolism , Cytokines/metabolism , Enzyme-Linked Immunosorbent Assay , Evoked Potentials, Auditory, Brain Stem/physiology , Female , Ginkgo biloba , HSP70 Heat-Shock Proteins/metabolism , Hearing Loss, Noise-Induced/metabolism , Hearing Loss, Noise-Induced/physiopathology , Heat Shock Transcription Factors/metabolism , Interleukin-1beta/drug effects , Interleukin-1beta/metabolism , Interleukin-6/metabolism , Random Allocation , Rats , Tumor Necrosis Factor-alpha/drug effects , Tumor Necrosis Factor-alpha/metabolismABSTRACT
CONCLUSION: Low-dose administration of Aspartame (Ap) did not produce a significant ototoxic effect at the end of the 6th month. However, duration of the ototoxic effect is shortened and severity of the effect is increased as dose and duration of Ap administration is increased. OBJECTIVES: While Ap toxicity has been studied in short- and long-term studies, its effects on hearing have not been investigated. This study was conducted to evaluate the effects of long-term consumption of Ap administered in various doses on hearing status of rats. METHODS: The study included 54 female Wistar Albino rats. Ap was given for 6 months to the rats. The groups were assigned according to levels of Ap dosage. DPOAE and ABR tests were utilized for serial hearing evaluations. Serial hearing measurement times were designed as baseline, 1st week, 2nd week, 1st, 2nd, 3rd, and 6th months. RESULTS: While audiological parameters deteriorated with 100 mg/kg/day dose after the 3rd month, ABR thresholds were elevated and DPOAE values were significantly decreased in 500 mg/kg/day and 1000 mg/kg/day applications after the 2nd month. In 2000 mg/kg/day and 4000 mg/kg/day applications, deteriorations in audiological parameters were detected as early as the first and second months; respectively.
Subject(s)
Aspartame/toxicity , Hearing/drug effects , Sweetening Agents/toxicity , Animals , Female , Rats , Rats, WistarABSTRACT
OBJECTIVES: The aim of this study was to evaluate audiologic properties of patients with Noonan syndrome and compare these findings with those of unaffected peers. METHODS: The study included 17 children with Noonan syndrome and 20 typically developing children without Noonan syndrome. Pure tone and speech audiometry, immitancemetric measurement, otoacoustic emissions measurement and auditory brainstem response tests were applied to all (n = 37) children. RESULTS: Hearing thresholds of children with Noonan syndrome were higher (poorer) than those observed unaffected peers, while the hearing sensitivity of the both groups were normal limits (p = 0.013 for right, p = 0.031 for left ear). Transient evoked otoacoustic emissions amplitudes of the children with Noonan syndrome were lower than the children without Noonan syndrome (p = 0.005 for right, p = 0.002 for left ear). Middle ear pressures and auditory brainstem response values were within normal limits and there was no difference between the two groups (p > 0.05). CONCLUSION: General benefit of the present study is to characterize the audiologic findings of children with Noonan syndrome, which is beneficial in clinics evaluating children with Noonan syndrome.
