Age-related oxidative decline of mitochondrial functions in rat brain is prevented by long term oral antioxidant supplementation
Age-related oxidative decline of mitochondrial functions in rat brain is prevented by long term oral antioxidant supplementation
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DOI：
10.1007/s10522-010-9301-8
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发表时间：
2011-04-01
期刊：
影响因子：
4.5
通讯作者：
Chakrabarti, Sasanka
中科院分区：
文献类型：
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作者：
Bagh, Maria Bindu;Thakurta, Ishita Guha;Chakrabarti, Sasanka
选择抗氧化剂（N-乙酰半胱氨酸、α-硫辛酸和α-生育酚）组合进行大鼠长期口服补充剂研究，以对大脑中与年龄相关的线粒体变化产生保护作用。选择四组大鼠：年轻对照组（6-7个月）；老年大鼠（22-24个月）；老年大鼠（22-24个月）从18个月起每天补充抗氧化剂，年轻大鼠（6-7个月）从2个月起每天补充抗氧化剂。测量四组大鼠脑线粒体功能参数、抗氧化酶状态和氧化损伤标志物积累。与年轻对照组相比，老年大鼠脑线粒体中复合物 IV 活性显着降低，跨膜电位和磷酸化能力丧失，同时氧化损伤标记物积累增加，抗氧化酶状态受损，但在补充口服抗氧化剂的老年大鼠中，线粒体改变在很大程度上被阻止。年轻大鼠的抗氧化剂补充对本研究中研究的线粒体参数没有影响。研究结果对衰老过程中大脑的生化和功能缺陷以及神经退行性疾病具有影响。
A combination of antioxidants (N-acetyl cysteine, alpha-lipoic acid, and alpha-tocopherol) was selected for long term oral supplementation study in rats for protective effects on age-related mitochondrial alterations in the brain. Four groups of rats were chosen: young control (6-7 months); aged rats (22-24 months); aged rats (22-24 months) on daily antioxidant supplementation from 18 month onwards and young rats (6-7 months) on daily antioxidant supplementation from 2 month onwards. The brain mitochondrial functional parameters, status of antioxidant enzymes and accumulation of oxidative damage markers were measured in the four groups of rats. A significant decrease in complex IV activity and a loss of transmembrane potential and phosphorylation capacity along with an increased accumulation of oxidative damage markers and compromised antioxidant enzyme status were noticed in aged rat brain mitochondria as compared to that in young controls, but in aged rats supplemented with oral antioxidants the mitochondrial alterations were largely prevented. Antioxidant supplementation in young rats had no effect on mitochondrial parameters investigated in this study. The results have implications in biochemical and functional deficits of brain during aging as well as in neurodegenerative disorders.