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小鼠心肌线粒体中与年龄和运动相关的变化

Age and exercise-related changes in myocardial mitochondria in mice.

作者信息

Coleman R, Weiss A, Finkelbrand S, Silbermann M

机构信息

Laboratory of Musculoskeletal Research, Rappaport Family Institute for Research in the Medical Sciences, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa.

出版信息

Acta Histochem. 1988;83(1):81-90. doi: 10.1016/S0065-1281(88)80075-8.

Abstract

A quantitative histochemical and an ultrastructural study was performed on the left ventricular myocardium of C57BL/6J female mice to evaluate the effects of aging and running exercise on mitochondrial structure and SDH activity. A comparison was made between 6-month-old ("young") and 27-month-old ("old") sedentary mice with age-matched mice subjected to running schedules (10 or 30 min/d) for 6 weeks. In longer-term studies, 27-month-old mice were given similar daily running schedules over a 10 month period ("long term runners"). No significant differences were found in SDH activity during the normal course of aging in mice (6 to 27 months of age), however, the response to running differed markedly in young versus old mice. "Young" trained mice showed significant increase in SDH activity compared with age-matched sedentary mice, whereas "old" trained mice showed significantly reduced SDH activity. Electron microscopy showed ultrastructural changes in mitochondria associated with aging including the development of large aggregations of mitochondria in subsarcolemmal and paranuclear sites. Running schedules, especially in aged runners, caused an increase in interfibrillar mitochondria hypertrophy, loss of matrix and cristae, incorporation of lipid inclusions and the formation of giant mitochondria. These abnormal mitochondrial changes are interpreted as being degenerative and possibly contributing to the reduced SDH levels found in cardiac myocytes of aged runners. Our results indicate that whereas regular exercise in young animals enhanced SDH activity, in aged mice it may be detrimental rather than beneficial.

摘要

对C57BL/6J雌性小鼠的左心室心肌进行了定量组织化学和超微结构研究,以评估衰老和跑步运动对线粒体结构和琥珀酸脱氢酶(SDH)活性的影响。将6个月大(“年轻”)和27个月大(“年老”)的久坐不动小鼠与年龄匹配且进行了6周跑步计划(每天10或30分钟)的小鼠进行比较。在长期研究中,给27个月大的小鼠在10个月期间安排类似的每日跑步计划(“长期跑步者”)。在小鼠正常衰老过程(6至27个月龄)中,未发现SDH活性有显著差异,然而,年轻小鼠和年老小鼠对跑步的反应明显不同。“年轻”的训练小鼠与年龄匹配的久坐不动小鼠相比,SDH活性显著增加,而“年老”的训练小鼠SDH活性显著降低。电子显微镜显示与衰老相关的线粒体超微结构变化,包括在肌膜下和核旁部位出现大量线粒体聚集。跑步计划,尤其是在老年跑步者中,导致肌原纤维间线粒体肥大增加、基质和嵴丢失、脂质包涵体形成以及巨型线粒体的形成。这些异常的线粒体变化被认为是退行性的,可能导致老年跑步者心肌细胞中SDH水平降低。我们的结果表明,虽然年轻动物定期运动可增强SDH活性,但在老年小鼠中,运动可能有害而非有益。

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