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1、Forever young? 青春永驻？BIOLOGISTS have made a lot of progress in understanding ageing. They have not, however, been able to do much about slowing it down. Particular versions of certain genes have been shown to prolong life, but that is no help to those who do not have them. A piece of work reported in
2、 this weeks Nature by Darren Baker of the Mayo Clinic, in Minnesota, though, describes an extraordinary result that points to a way the process might be ameliorated. Dr Baker has shownin mice, at leastthat ageing body cells not only suffer themselves, but also have adverse effects on otherwise healt
3、hy cells around them. More significantly, he has shown that if such ageing cells are selectively destroyed, these adverse effects go away. 在对人类衰老过程的探索中生物学家们取得了长足的进步。可是如何减缓衰老他们还没有太多的办法。与延长寿命相关的特定基因已经找到，但这还帮不了那些此段基因缺失的人。本周自然杂志发表了明尼苏达州梅奥诊所的 Dr.Darren Baker 的一项实验报告，描述了其所采取的方法使得衰老进程得到改善，结果非常好。至少在实验小白鼠体内是
4、这样，Dr.Barker 称体细胞不仅自己逐渐衰老,还将不利的影响传达到周围健康的细胞。更神奇的是，如果这些衰老的细胞被人为破坏掉，它们对健康细胞的负面影响也会随之消失。The story starts with an observation, made a few years ago, that senescent cells often produce a molecule called P16INK4A. Most body cells have an upper limit on the number of times they can divideand thus multiply
5、in number. P16INK4A is part of the control mechanism that brings cell division to a halt when this limit is reached. 故事还得从几年前的一项实验开始讲起，他们观察到衰老的细胞通常会产生一种叫 P16INK4A 的分子。大部分体细胞分裂次数会有一个上限数量的翻倍，当这个上限接近时，P16INK4A 作为控制机制的一部分会使细胞的分裂停止。The Hayflick limit(1), as the upper bound is known (after Leonard Hayflic
6、k, the biologist who discovered it), is believed to be an anticancer mechanism. It provides a backstop that prevents a runaway cell line from reproducing indefinitely, and thus becoming a tumour. The limit varies from species to speciesin humans, it is about 60 divisionsand its size is correlated wi
7、th the lifespan of the animal concerned. Hayflick-limited cells thus accumulate as an animal ages, and many biologists believe they are one of the things which control maximum lifespan. Dr Bakers experiment suggests this is correct. 海弗利克极限，即我们所知的上限（以发现的生物学家 Leonard Hayflick 的名字命名）现在认为可作为一种抗癌机制，它可以拦截
8、、阻断细胞链的无限期、失常的增生，正是这种失常的增生形成了肿瘤。这种极限随物种不同而不同，人类大致的分裂次数上限是 60 次，极限的大小与相应动物的预期生命期限有关。 细胞的海弗利克极限累加就是动物的寿命长度，很多的生物学家推测它们控制着生命期限最长值。Dr.Barker 的实验证明了推测是正确的。Age shall not weary them 老而未衰的器官Dr Baker genetically engineered a group of mice that were already quite unusual. They had a condition called progeria,
9、 meaning that they aged much more rapidly than normal mice. (A few unfortunate humans suffer from a similar condition.) The extra tweak he added to the DNA of these mice was a way of killing cells that produce P16INK4A. He did this by inserting into the animals DNA, near the gene for P16INK4A, a sec
10、ond gene that was, because of this proximity, controlled by the same genetic switch. This second gene, activated whenever the gene for P16INK4A was active, produced a protein that was harmless in itself, but which could be made deadly by the presence of a particular drug. Giving a mouse this drug, t
11、hen, would kill cells which had reached their Hayflick limits while leaving other cells untouched. Dr Baker raised his mice, administered the drug, and watched. Dr. Baker 通过基因工程处理的一组小白鼠非常特别，它们的症状也称早老症，意味着它们比一般的小白鼠衰老的更快。（不幸的是，少数人类也患有这一病症），他在这些小白鼠的 DNA 中加入了可杀死能产生 P16INK4A 分子的细胞的特别基因，具体做法是在实验小白鼠 P16INK
12、4A 旁边的基因插入另一段动物基因，因为在它旁边，第二段基因也受相同的遗传开关控制。这第二段基因编码产生的蛋白质对自身无害，但在特殊的药物作用下，它就会变的很致命，只要 P16INK4A 分子有活性它就能被激活。给实验小白鼠服用这种药后，就会杀死那些接近海弗利克极限的细胞，其它细胞则完好无损。Dr Baker 培养这些小白鼠,给它们服用药物后，观察它们。The results were spectacular. Mice given the drug every three days from birth suffered far less age-related body-wasting t
13、han those which were not. They lost less fatty tissue. Their muscles remained plump (and effective, too, according to treadmill tests). And they did not suffer cataracts of the eye. They did, though, continue to experience age-related problems in tissues that do not produce P16INK4A as they get old.
14、 In particular, their hearts and blood vessels aged normally (or, rather, what passes for normally in mice with progeria). For that reason, since heart failure is the main cause of death in such mice, their lifespans were not extended. 结果是出人意料的。小白鼠出生后每 3 天给一次药,服药小白鼠比没服药小白鼠的与衰老相关的机体耗损要少的多。它们耗损的脂肪组织更少
15、，肌肉丰满(经过反复实验，效果都不错),并且都没患上白内障。接下来，他们还对那些老化的但并没有出现 P16INK4A 分子的器官也进行了衰老相关问题的实验，特别是它们的心脏和血管，老化的进程很正常（即使患早老症的小白鼠也是这样），小白鼠的主要是死因心脏衰竭，所以它们的预期寿命不会再延长了。The drug, Dr Baker found, produced some benefit even if it was administered to a mouse only later in life. Though it could not clear cataracts that had alr
16、eady formed, it partly reversed muscle- wasting and fatty-tissue loss. Such mice were thus healthier than their untreated confrres. Dr Baker 发现，这种药物即使是饲喂给生命快到尽头的的小白鼠也会有一定的疗效，尽管对已经形成的白内障没法再变回清澈，但能使肌肉及脂肪组织的耗损部分得以缓解，这些小白鼠因此比没有服药的更健康。Analysis of tissue from mice killed during the course of the experiment showed that the drug was having its intended effect. Cells producing P16INK4A were killed and cleared away as they appeared. Dr Baker
