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Mn-SOD 杂合子敲除小鼠的年龄相关性听力损失。

Age-related hearing loss in Mn-SOD heterozygous knockout mice.

机构信息

Department of Otolaryngology and Head and Neck Surgery, University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-8665, Japan.

出版信息

Oxid Med Cell Longev. 2013;2013:325702. doi: 10.1155/2013/325702. Epub 2013 Jun 27.

DOI:10.1155/2013/325702
PMID:23936608
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3710654/
Abstract

Age-related hearing loss (AHL) reduces the quality of life for many elderly individuals. Manganese superoxide dismutase (Mn-SOD), one of the antioxidant enzymes acting within the mitochondria, plays a crucial role in scavenging reactive oxygen species (ROS). To determine whether reduction in Mn-SOD accelerates AHL, we evaluated auditory function in Mn-SOD heterozygous knockout (HET) mice and their littermate wild-type (WT) C57BL/6 mice by means of auditory brainstem response (ABR). Mean ABR thresholds were significantly increased at 16 months when compared to those at 4 months in both WT and HET mice, but they did not significantly differ between them at either age. The extent of hair cell loss, spiral ganglion cell density, and thickness of the stria vascularis also did not differ between WT and HET mice at either age. At 16 months, immunoreactivity of 8-hydroxydeoxyguanosine was significantly greater in the SGC and SV in HET mice compared to WT mice, but that of 4-hydroxynonenal did not differ between them. These findings suggest that, although decrease of Mn-SOD by half may increase oxidative stress in the cochlea to some extent, it may not be sufficient to accelerate age-related cochlear damage under physiological aging process.

摘要

年龄相关性听力损失(AHL)降低了许多老年人的生活质量。锰超氧化物歧化酶(Mn-SOD)是线粒体中一种抗氧化酶,在清除活性氧(ROS)方面起着至关重要的作用。为了确定 Mn-SOD 的减少是否会加速 AHL,我们通过听觉脑干反应(ABR)评估了 Mn-SOD 杂合敲除(HET)小鼠及其同窝野生型(WT)C57BL/6 小鼠的听觉功能。与 4 个月时相比,WT 和 HET 小鼠在 16 个月时的平均 ABR 阈值均显著升高,但在两个年龄组之间无显著差异。WT 和 HET 小鼠在两个年龄组之间的毛细胞丢失程度、螺旋神经节细胞密度和血管纹厚度也无差异。在 16 个月时,与 WT 小鼠相比,HET 小鼠的 SGC 和 SV 中 8-羟基脱氧鸟苷的免疫反应性显著增加,但 4-羟基壬烯醛的免疫反应性在两组之间没有差异。这些发现表明,尽管 Mn-SOD 减少一半可能会在一定程度上增加耳蜗中的氧化应激,但在生理老化过程中,这可能不足以加速与年龄相关的耳蜗损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/560b665c307b/OXIMED2013-325702.012.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/560b665c307b/OXIMED2013-325702.012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/20cc613d4a92/OXIMED2013-325702.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/7dc06b7fe939/OXIMED2013-325702.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/568ed72a2ef5/OXIMED2013-325702.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/1f0c4984fed0/OXIMED2013-325702.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/b20e2255be22/OXIMED2013-325702.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/4334b240cbe2/OXIMED2013-325702.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/cf36bb72d4da/OXIMED2013-325702.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/998ad9b004e0/OXIMED2013-325702.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/728d5efecb97/OXIMED2013-325702.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/bcd39152dc9c/OXIMED2013-325702.010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/939676f7b501/OXIMED2013-325702.011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/017b/3710654/560b665c307b/OXIMED2013-325702.012.jpg

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