如果你覺得外面的空氣是受到污染的,，那么Genetics雜志9月份的一篇研究報告可能會使你思考我們體內(nèi)的空氣同樣也是受到污染的,。研究人員發(fā)現(xiàn)我們吸進(jìn)的3%的空氣會轉(zhuǎn)化成有害的過氧化物，并最終會對肌肉造成損害,。
過氧化物會導(dǎo)致一種叫活性氧（ROS）的分子產(chǎn)生,，這種分子對肌肉組織尤其有害。ROS可能導(dǎo)致嚴(yán)重的問題,，從老齡化到帕金森疾病和癌癥,。
研究人員介紹說，他們希望這項研究能夠引導(dǎo)一個關(guān)于老年人不可避免的身體機(jī)能衰退,，和其他年齡相關(guān)的衰弱的研究的新方向,。
Duttaroy和同事先前研究表明在果蠅和老鼠體內(nèi)ROS導(dǎo)致的細(xì)胞破壞是一樣的,。剛開始，他們使用體內(nèi)沒有線粒體超氧化物歧化酶（SOD）的果蠅進(jìn)行試驗,。結(jié)果表明缺乏SOD的果蠅在孵化后一天就死亡,。然后通過遺傳操作，研究人員分別在神經(jīng)和肌肉組織中激活了SOD的生成,，發(fā)現(xiàn)在神經(jīng)組織中,，SOD對延長果蠅生命沒有明顯差異，但是在肌肉組織中卻有明顯的不同,。肌肉中有SOD生成的果蠅其存活率明顯上升,，幾天后它們可以和正常的個體一樣活動。對肌肉活性的測量同樣表明SOD有助于肌肉正常的運(yùn)作,。
長期的觀點認(rèn)為我們吸進(jìn)的氧是有毒的,，而這項研究為這一觀點提供了明確的實例，并闡明了其嚴(yán)重的后果,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
