隨著年齡的增長,，一種分子在人體中的濃度會(huì)自然減少,，然而，科學(xué)家們發(fā)現(xiàn),，通過對這種分子實(shí)施管理,，則可以顯著提高細(xì)胞的壽命。新發(fā)現(xiàn)發(fā)表在《自然—細(xì)胞生物學(xué)》期刊上,，清楚地顯示出通過何種努力可以延長某種特定細(xì)胞的生命,。
老化與哺乳類細(xì)胞的多種生物化學(xué)變化相關(guān)，比如一種名為亞精胺的分子在細(xì)胞中的減少,。亞精胺是一種多胺化合物,，存在于核糖體及活組織中，具有各種代謝功能,，與細(xì)胞的生長和成長有關(guān),，然而,，科學(xué)家們一直不清楚這種細(xì)胞的數(shù)量減少究竟是老化的原因呢,，還是老化的結(jié)果。
Frank Madeo和同事發(fā)現(xiàn),，對果蠅,、線蟲和酵母體內(nèi)的亞精胺實(shí)施管理，可提高這些生物的壽命,。同樣地,，他們發(fā)現(xiàn)在培養(yǎng)液中加入額外的亞精胺可以延長人類細(xì)胞的壽命。這些發(fā)現(xiàn)顯示,，亞精胺能延長細(xì)胞的壽命,，而且最終延長組織的壽命，因?yàn)樗鼈兲峁┝肆硪环N清掃細(xì)胞的機(jī)制：不再是破壞細(xì)胞機(jī)制讓細(xì)胞程序化死亡,，亞精胺實(shí)際上是一種通道,，讓不必要且有潛在危險(xiǎn)的細(xì)胞喪失功能。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature Cell Biology 11, 1305 - 1314 (2009) 4 October 2009 | doi:10.1038/ncb1975
Induction of autophagy by spermidine promotes longevity
Tobias Eisenberg1, Heide Knauer1, Alexandra Schauer1, Sabrina Büttner1, Christoph Ruckenstuhl1, Didac Carmona-Gutierrez1, Julia Ring1, Sabrina Schroeder1, Christoph Magnes2, Lucia Antonacci1, Heike Fussi1, Luiza Deszcz3,4, Regina Hartl3,4, Elisabeth Schraml5, Alfredo Criollo6,7,8, Evgenia Megalou9, Daniela Weiskopf10, Peter Laun11, Gino Heeren11, Michael Breitenbach11, Beatrix Grubeck-Loebenstein10, Eva Herker12, Birthe Fahrenkrog13, Kai-Uwe Fr?hlich1, Frank Sinner2, Nektarios Tavernarakis9, Nadege Minois3,4,14, Guido Kroemer6,7,8 & Frank Madeo1
Ageing results from complex genetically and epigenetically programmed processes that are elicited in part by noxious or stressful events that cause programmed cell death. Here, we report that administration of spermidine, a natural polyamine whose intracellular concentration declines during human ageing, markedly extended the lifespan of yeast, flies and worms, and human immune cells. In addition, spermidine administration potently inhibited oxidative stress in ageing mice. In ageing yeast, spermidine treatment triggered epigenetic deacetylation of histone H3 through inhibition of histone acetyltransferases (HAT), suppressing oxidative stress and necrosis. Conversely, depletion of endogenous polyamines led to hyperacetylation, generation of reactive oxygen species, early necrotic death and decreased lifespan. The altered acetylation status of the chromatin led to significant upregulation of various autophagy-related transcripts, triggering autophagy in yeast, flies, worms and human cells. Finally, we found that enhanced autophagy is crucial for polyamine-induced suppression of necrosis and enhanced longevity.
1 Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria.
2 Institute of Medical Technologies and Health Management, Joanneum Research, Graz, Austria.
3 Research Institute of Molecular Pathology (IMP), Vienna, Austria.
4 Institute of Molecular Biotechnology (IMBA), Austrian Academy of Sciences, Vienna, Austria.
5 Institute of Applied Microbiology, University of Natural Resources and Applied Life Sciences, Vienna, Austria.
6 INSERM, U848; 94805 Villejuif, France.
7 Institut Gustave Roussy, 94805 Villejuif, France.
8 University Paris Sud, Paris-11, 94805 Villejuif, France.
9 Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, 70013, Heraklion, Crete, Greece.
10 Institute for Biomedical Ageing Research, Austrian Academy of Sciences, 6020 Innsbruck, Austria.
11 Department of Cell Biology, Division of Genetics, University of Salzburg, 5020 Salzburg, Austria.
12 Gladstone Institute of Virology and Immunology, San Francisco, CA 94158, USA.
13 M.E. Mueller Institute for Structural Biology, Biozentrum, University of Basel, 4056 Basel, Switzerland.
14 Current address: School of Biology, University of St Andrews, St Andrews, Scotland, Fife KY16 9AJ, UK.
