為什么人類會隨著年老而喪失活力，體內(nèi)堆積越來越多的垃圾？據(jù)美國物理學家組織網(wǎng)8月30日報道，美國南加利福尼亞大學生物學家最近發(fā)現(xiàn)，隨著細胞老化，它們調(diào)動一種天然抗氧化劑——Lon蛋白酶的能力會大大下降，而Lon蛋白酶負責把損壞的蛋白質(zhì)分解并清除掉。該發(fā)現(xiàn)有助于制定合理的飲食結(jié)構(gòu)，開發(fā)延緩衰老過程的新藥。研究論文發(fā)表在最近出版的《老年醫(yī)學期刊》（The Journals of Gerontology ）上。
Impairment of Lon-Induced Protection Against the Accumulation of Oxidized Proteins in Senescent Wi-38 Fibroblasts
Jenny K. Ngo1,2, Laura C. D. Pomatto1, Daniela A. Bota3, Alison L. Koop1 and Kelvin J. A. Davies1,2
Oxidative damage to mitochondrial proteins is thought to contribute to the aging process, but the Lon protease normally degrades such proteins. In early-passage WI-38 human lung fibroblasts, Lon expression is rapidly induced during H2O2 stress, which prevents the accumulation of oxidized proteins and protects cell viability. In contrast, middle passage cells exhibit only sluggish induction of Lon expression in oxidative stress, and oxidized proteins initially accumulate. Late-passage, or senescent, cells have low basal levels of Lon and high levels of accumulated oxidized proteins; in response to oxidative stress, they fail to induce Lon expression and exhibit continually increasing accumulation of oxidized proteins. Senescent cells separated into two populations, one exhibiting normal mitochondrial mass and a second displaying significant loss of mitochondria; both populations had diminished mitochondrial transmembrane potential. These senescent changes are similar to the effects of Lon silencing in young cells. We suggest that loss of Lon stress inducibility is part of a pattern of diminishing stress adaptability that predisposes cells to senescence.
為什么人類會隨著年老而喪失活力，體內(nèi)堆積越來越多的垃圾？據(jù)美國物理學家組織網(wǎng)8月30日報道，美國南加利福尼亞大學生物學家最近發(fā)現(xiàn)，隨著細胞老化，它們調(diào)動一種天然抗氧化劑——Lon蛋白酶的能力會大大下降，而Lon蛋白酶負責把損壞的蛋白質(zhì)分解并清除掉。該發(fā)現(xiàn)有助于制定合理的飲食結(jié)構(gòu)，開發(fā)延緩