如果你觉得外面的空气是受到污染的，那么Genetics杂志9月份的一篇研究报告可能会使你思考我们体内的空气同样也是受到污染的。研究人员发现我们吸进的3%的空气会转化成有害的过氧化物，并最终会对肌肉造成损害。
过氧化物会导致一种叫活性氧（ROS）的分子产生，这种分子对肌肉组织尤其有害。ROS可能导致严重的问题，从老龄化到帕金森疾病和癌症。
研究人员介绍说，他们希望这项研究能够引导一个关于老年人不可避免的身体机能衰退，和其他年龄相关的衰弱的研究的新方向。
Duttaroy和同事先前研究表明在果蝇和老鼠体内ROS导致的细胞破坏是一样的。刚开始，他们使用体内没有线粒体超氧化物歧化酶（SOD）的果蝇进行试验。结果表明缺乏SOD的果蝇在孵化后一天就死亡。然后通过遗传操作，研究人员分别在神经和肌肉组织中激活了SOD的生成，发现在神经组织中，SOD对延长果蝇生命没有明显差异，但是在肌肉组织中却有明显的不同。肌肉中有SOD生成的果蝇其存活率明显上升，几天后它们可以和正常的个体一样活动。对肌肉活性的测量同样表明SOD有助于肌肉正常的运作。
长期的观点认为我们吸进的氧是有毒的，而这项研究为这一观点提供了明确的实例，并阐明了其严重的后果。（生物谷Bioon.com）
生物谷推荐原始出处：
Genetics, Vol. 183, 175-184, September 2009,doi:10.1534/genetics.109.103515
Mitochondrial Superoxide Radicals Differentially Affect Muscle Activity and Neural Function
Tanja Godenschwege*,1, Renée Forde,1, Claudette P. Davis, Anirban Paul,2, Kristopher Beckwith and Atanu Duttaroy,3
* Department of Biological Sciences, Florida Atlantic University, Boca Raton, Florida 33431 and Biology Department, Howard University, Washington, DC 20059
3 Corresponding author: Biology Department, Howard University, 415 College St., NW, Washington, DC 20059.
Cellular superoxide radicals (O2–) are mostly generated during mitochondrial oxygen metabolism. O2– serves as the raw material for many reactive oxygen species (ROS) members like H2O2 and OH.– radicals following its catalysis by superoxide dismutase (SOD) enzymes and also by autocatalysis (autodismutation) reactions. Mitochondrial ROS generation could have serious implications on degenerative diseases. In model systems overproduction of mitochondrial O2–resulting from the loss of SOD2 function leads to movement disorders and drastic reduction in life span in vertebrates and invertebrates alike. With the help of a mitochondrial SOD2 loss-of-functionmutant, Sod2n283, we measured the sensitivity of muscles and neurons to ROS attack. Neural outputs from flight motor neurons and sensory neurons were unchanged in Sod2n283 and the entire neural circuitry between the giant fiber (GF) and the dorsal longitudinal muscles (DLM) showed no overt defect due to elevated ROS. Such insensitivity of neurons to mitochondrial superoxides was further established through neuronal expression of SOD2, which failed to improve survival or locomotive ability of Sod2n283. On the other hand, ultrastructural analysis ofSod2n283 muscles revealed fewer mitochondria and reduced muscle ATP production. By targeting the SOD2 expression to the muscle we demonstrate that the early mortality phenotype of Sod2n283can be ameliorated along with signs of improved mobility. In summary, muscles appear to be more sensitive to superoxide attack relative to the neurons and such overt phenotypes observed in SOD2-deficient animals can be directly attributed to the muscle.
