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热量限制对啮齿动物和恒河猴年龄相关性听力损失的影响。

Effects of caloric restriction on age-related hearing loss in rodents and rhesus monkeys.

作者信息

Someya Shinichi, Tanokura Masaru, Weindruch Richard, Prolla Tomas A, Yamasoba Tatsuya

机构信息

Departments of Genetics & Medical Genetics, University of Wisconsin, Madison, WI 53706, USA.

出版信息

Curr Aging Sci. 2010 Feb;3(1):20-5. doi: 10.2174/1874609811003010020.

Abstract

Age-related hearing loss (AHL), also known as presbycusis, is a universal feature of mammalian aging and is the most frequently occurring sensory disorder in the elderly population. AHL is characterized by a decline of auditory function and loss of hair cells and spiral ganglion neurons in the cochlea of the inner ear. It has been postulated that AHL occurs gradually as a result of the cumulative effect with aging of exposure to noise, diet, oxidative damage, and mitochondrial DNA mutations. However, the molecular mechanisms of AHL remain unclear and no preventative or therapeutic interventions have been developed. A growing body of evidence suggests increased oxidative damage with aging to macromolecules such as DNA, proteins, and lipids may play a causal role in aging and age-related diseases. Caloric restriction (CR) extends the lifespan of most mammalian species, delays the onset of multiple age-related diseases, and attenuates both the degree of oxidative damage and the associated decline in physiological function. Here, we review studies on CR's ability to prevent cochlear pathology and AHL in laboratory animals and discuss potential molecular mechanisms of CR's actions.

摘要

年龄相关性听力损失(AHL),也称为老年性聋,是哺乳动物衰老的普遍特征,也是老年人群中最常见的感觉障碍。AHL的特征是听觉功能下降以及内耳耳蜗中的毛细胞和螺旋神经节神经元丧失。据推测,AHL是由于噪声暴露、饮食、氧化损伤和线粒体DNA突变等因素随年龄增长的累积效应而逐渐发生的。然而,AHL的分子机制仍不清楚,尚未开发出预防性或治疗性干预措施。越来越多的证据表明,随着年龄增长,DNA、蛋白质和脂质等大分子的氧化损伤增加可能在衰老和年龄相关性疾病中起因果作用。热量限制(CR)可延长大多数哺乳动物物种的寿命,延迟多种年龄相关性疾病的发生,并减轻氧化损伤程度和相关生理功能下降。在此,我们综述了关于CR预防实验动物耳蜗病变和AHL能力的研究,并讨论了CR作用的潜在分子机制。

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