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Effects of ascorbic acid on oxidative system and transient evoked otoacoustic emissions in rabbits exposed to noise.

机译:抗坏血酸对暴露于噪音的家兔氧化系统和短暂诱发耳声发射的影响。

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OBJECTIVES/HYPOTHESIS: The objective was to investigate the effects of both noise exposure and ascorbic acid on oxidative status and hearing thresholds of rabbits. STUDY DESIGN: Randomized prospective animal study comparing oxidative parameters and otoacoustic emissions in two rabbit groups exposed to noise. One group was given ascorbic acid, the other group was not given any treatment. METHODS: Two groups of rabbits were used in the study; each group had six rabbits. The six rabbits in the first group were not given any treatment, whereas 500 mg intramuscular ascorbic acid twice daily for 2 1/2 days was given to the six rabbits in the second group. Transient evoked otoacoustic emissions were recorded in all animals before and after noise exposure. Total protein sulfhydryl groups, carbonyl contents, and malondialdehyde levels, as well as erythrocyte glutathione, superoxide dismutase, and catalase enzyme levels, were measured in all rabbits. All the rabbits were exposed to noise (100 dB sound pressure level, 1000 Hz, 1 h), and transient evoked otoacoustic emissions were recorded again. RESULTS: When oxidative parameters before noise exposure were compared, erythrocyte glutathione and catalase enzyme levels were detected to be higher in the second group (P <.05). In the first group of rabbits after noise exposure, total protein sulfhydryl groups were found to be reduced (P <.05), whereas plasma carbonyl contents and malondialdehyde levels were elevated significantly (P <.05). In this group, erythrocyte glutathione, superoxide dismutase, and catalase enzyme levels were low (P <.05). In the second group, which was given ascorbic acid, total protein sulfhydryl groups were reduced (P <.05), whereas plasma carbonyl contents and malondialdehyde levels did not change (P >.05) following noise exposure. In the second group, erythrocyte glutathione and catalase enzyme levels were reduced (P <.05), but superoxide dismutase levels did not change (P >.05). Transient evoked otoacoustic emissions after noise exposure wereweak in both groups, but reproducibility and signal-to-noise ratios were higher in the second group (P <.05). CONCLUSION: Ascorbic acid treatment inhibited both lipid peroxidation and oxidative damage of proteins in rabbits exposed to noise. The study data suggest, at least, that oxidative status should be included in the physiopathology of noise-induced hearing loss; in addition, a brief application of ascorbic acid before noise exposure appeared to play a protective role for cochlea.
机译:目的/假设:目的是研究噪声暴露和抗坏血酸对家兔氧化状态和听力阈值的影响。研究设计:随机前瞻性动物研究,比较了暴露于噪音的两个兔子组的氧化参数和耳声发射。一组接受抗坏血酸治疗,另一组未接受任何治疗。方法:采用两组兔子进行研究。每组有六只兔子。第一组中的六只兔子未接受任何治疗,而第二组中的六只兔子则每天两次两次服用500 mg肌内抗坏血酸,持续2 1/2天。在噪声暴露之前和之后,在所有动物中记录了瞬态诱发的耳声发射。测量了所有兔子的总蛋白质巯基,羰基含量和丙二醛水平,以及红细胞谷胱甘肽,超氧化物歧化酶和过氧化氢酶水平。将所有兔子暴露于噪声(100 dB声压级,1000 Hz,1 h)下,并再次记录瞬态诱发的耳声发射。结果:当比较噪声暴露前的氧化参数时,第二组的红细胞谷胱甘肽和过氧化氢酶水平较高(P <.05)。在噪声暴露后的第一组兔子中,总蛋白质巯基被发现减少(P <.05),而血浆羰基含量和丙二醛水平显着升高(P <.05)。在该组中,红细胞谷胱甘肽,超氧化物歧化酶和过氧化氢酶水平较低(P <.05)。在给予抗坏血酸的第二组中,总蛋白质巯基基团减少了(P <.05),而暴露于噪音后血浆羰基含量和丙二醛水平没有变化(P> .05)。在第二组中,红细胞谷胱甘肽和过氧化氢酶水平降低(P <.05),但超氧化物歧化酶水平没有变化(P> .05)。两组噪声暴露后的瞬态诱发耳声发射均较弱,但第二组的再现性和信噪比较高(P <.05)。结论:抗坏血酸处理可抑制家兔噪声中脂质过氧化和蛋白质的氧化损伤。研究数据至少表明,氧化状态应包括在噪声诱发的听力损失的生理病理学中。另外,在噪声暴露前短暂应用抗坏血酸似乎对耳蜗起保护作用。

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