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   2020| July-September  | Volume 22 | Issue 106  
    Online since December 31, 2020

 
 
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ORIGINAL ARTICLES
Adrenergic alpha-2 receptor antagonists cease augmented oxidation of plasma proteins and anxiety of rats caused by chronic noise exposure
Ashkhen Lyova Manukyan, Artem Sergey Grigoryan, Lilit Serob Hunanyan, Hayk Ashot Harutyunyan, Mariam Varos Manukyan, Magdalina Mher Melkonyan
July-September 2020, 22(106):63-69
DOI:10.4103/nah.NAH_31_19  
Background: Noise is one of the environmental factors, which is considered as a powerful stressor for the organism. Generally, the acoustic stress affects the behavior and physiological state of humans and animals. Aims: The goal of this study is to investigate the relationship between chronic noise exposure and the effects of adrenergic alpha-2 receptor antagonists, beditin and mesedin, on the anxiety and oxidation of plasma proteins and fibrinogen in rats. Methods: The experiments were carried out on non-linear albino male rats, divided into four groups (six animals in each): 1. Healthy controls 2. Exposed to noise of a level 91 dB(A), eight hours daily, during 7, 30 and 60 days; 3. Injected with 2 mg/kg of beditin (2-(2-amino-4-thiazolyl)-1,4-benzodioxane hydrochloride)); 4. Injected with 10 mg/kg mesedin (2-(2-methyl-amino-thiozolyl)-1,4-benzodioxane hydrochloride). For evaluating the cognitive impairment, the Any-maze test was applied. The level of carbonylation of proteins was assessed by reaction with 2,4-dinitrophenylhydrazine, spectrophotometrically. Results: Chronic noise decreased locomotor activity and increased anxiety and oxidation of plasma protein and fibrinogen. Intensity of these changes were dependent on the duration of noise exposure. Conclusion: The Alpha 2 adrenoblockers alleviate oxidative modification of plasma proteins and reduce the cognitive impairment caused by chronic exposure to noise.
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The effects of hyperinsulinemia on cochlear functions
Arzu Or Koca, Hüseyin Samet Koca, Cüneyd Anil
July-September 2020, 22(106):70-76
DOI:10.4103/nah.NAH_41_20  PMID:33402607
Context: Hyperinsulinemia is the most common metabolic change associated with cochleovestibular diseases. Aim: We aimed to investigate the auditory functions in hyperinsulinemic individuals. Settings and Design: A total of 164 patients were included in this case-control study. While 76 patients with insulin resistance (homeostasis model assessment of insulin resistance [HOMA-IR] of ≥2.5) constituted the case group, 88 patients with HOMA-IR values of <2.5 constituted the control group of the study. Material and Methods: The 75 g oral glucose tolerance test, blood biochemistry tests, hormonal analysis, audiological assessment, electrocochleography (EcochG), and transient evoked otoacoustic emissions (TEOAE) testing were performed. Statistical Analysis: One-way analysis of variance and Kruskal–Wallis analysis of variance were used for the comparison of the metabolic and ear parameters in the normal glucose tolerance (NGT), impaired fasting glucose (IFG), and impaired glucose tolerance (IGT) groups. The chi-square test was used to compare nominal variables. Spearman and Pearson correlation coefficients were used for the correlation analyses of continuous variables. Results: The pure tone audiometry at 0.5, 1, 2, and 4 kHz was better in the case group than in the control group. A positive correlation was found between HbA1c and right ear 0.5, 1, 4, and 8 kHz threshold values and left ear 2, 4, 6, and 8 kHz threshold values. A negative correlation was found between HbA1c and speech discrimination scores. The right ear 1.00 and 2.83 kHz TEOAE measurements in the individuals with NGT were found higher than those in patients with IGT, and the 1.42 kHz TEOAE measurements and reproducibility were found higher than those in patients with IFG. The left ear 1.00 and 1.42 kHz TEOAE measurements of the IGT patients were found lower than those of IFG and NGT patients. Conclusion: We showed that hearing was worsening in hyperinsulinemic patients and prediabetic conditions were related to hearing function impairment.
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