Chronic melatonin treatment prevents age-dependent cardiac mitochondrial dysfunction in senescence-accelerated mice
Chronic melatonin treatment prevents age-dependent cardiac mitochondrial dysfunction in senescence-accelerated mice
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DOI：
10.1080/10715760600936359
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发表时间：
2007-01-01
影响因子：
3.3
通讯作者：
Acuna-Castroviejo, Dario
中科院分区：
文献类型：
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作者：
Rodriguez, Maria I.;Carreterop, Miguel;Acuna-Castroviejo, Dario
对5月龄和10月龄雌性加速衰老(SAMP8)和抗衰老(SAMR1)小鼠的心脏线粒体进行了研究。通过测定线粒体脂质过氧化、谷胱甘肽和谷胱甘肽二硫键、谷胱甘肽过氧化物酶和还原酶活性来确定线粒体氧化应激程度。通过测定呼吸链复合体活性和三磷酸腺苷含量来评价线粒体功能。结果表明，SAMP8小鼠心脏线粒体氧化损伤与年龄相关，伴随着电子传递链复合体活性和ATP水平的降低。在1至10个月龄期间长期服用褪黑素可使线粒体的氧化还原和生物能量状态正常化，并提高ATP水平。这些结果支持在10个月大的SAM小鼠中存在显著的线粒体氧化应激，并且它们表明了褪黑素的长期药物干预的有益效果，褪黑素可以减少心肌线粒体随年龄的恶化和功能性氧化变化。
Heart mitochondria from female senescence-accelerated (SAMP8) and senescence-resistant (SAMR1) mice of 5 or 10 months of age, were studied. Mitochondrial oxidative stress was determined by measuring the levels of lipid peroxidation, glutathione and glutathione disulfide and glutathione peroxidase and reductase activities. Mitochondrial function was assessed by measuring the activity of the respiratory chain complexes and ATP content. The results show that the age-dependent mitochondrial oxidative damage in the heart of SAMP8 mice was accompanied by a reduction in the electron transport chain complex activities and in ATP levels. Chronic melatonin administration between 1 and 10 months of age normalized the redox and the bioenergetic status of the mitochondria and increased ATP levels. The results support the presence of significant mitochondrial oxidative stress in SAM mice at 10 months of age, and they suggest a beneficial effect of chronic pharmacological intervention with melatonin, which reduces the deteriorative and functional oxidative changes in cardiac mitochondria with age.