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Recharging mitochondrial batteries in old eyes. Near infra-red increases ATP

机译:为老眼中的线粒体电池充电。近红外增加ATP

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Progressive accumulation of age related mitochondrial DNA mutations reduce ATP production and increase reactive oxygen species output, leading to oxidative stress, inflammation and degradation. The pace of this is linked to metabolic demand. The retina has the greatest metabolic demand and mitochondrial density in the body and displays progressive age related inflammation and marked cell loss. Near infra-red (670 nm) is thought to be absorbed by cytochrome c oxidase (COX), a key element in mitochondrial respiration and it has been demonstrated that it improves mitochondrial membrane potentials in aged eyes. It also significantly reduces the impact of experimental pathology and ameliorates age related retinal inflammation. We show ATP decline with ageing in mouse retina and brain. Also, in these tissues that ATP is significantly increased by 670 nm exposure in old mice. In the retina this was associated with increased COX and reduced acrolein expression. Acrolein, being a free radical marker of retinal oxidative stress, is up regulated in Alzheimer's and retinal degeneration. This is the first demonstration of ATP manipulation in vivo and may provide a simple non-invasive route to combating age related tissue decline.
机译:与年龄相关的线粒体DNA突变的逐步积累减少了ATP的产生并增加了活性氧的输出,从而导致氧化应激,炎症和降解。其速度与代谢需求有关。视网膜在体内具有最大的代谢需求和线粒体密度,并显示出与年龄有关的进行性炎症和明显的细胞丢失。人们认为,近红外(670 nm)被细胞色素c氧化酶(COX)吸收,这是线粒体呼吸作用的关键因素,并且已证明它可以改善老年眼睛的线粒体膜电位。它还显着降低了实验病理学的影响,并改善了与年龄有关的视网膜炎症。我们显示随着小鼠视网膜和大脑衰老,ATP下降。同样,在这些组织中,老年小鼠的670 nm暴露使ATP显着增加。在视网膜中,这与COX增加和丙烯醛表达降低有关。丙烯醛是视网膜氧化应激的自由基标记,在阿尔茨海默氏病和视网膜变性中被上调。这是体内ATP操纵的第一个证明,并且可以提供一种简单的非侵入性途径来对抗与年龄相关的组织衰退。

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