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Over the last few decades, scientists have described some hypotheses explaining how stress can accelerate aging.
在过去的几十年里，科学家们提出一些假说解释压力如何加速衰老。
And a new study published in Molecular Cell this week from the University of Pittsburgh
本周匹兹堡大学发表于《Molecular Cell》上的一项研究
provided the first direct evidence of one of those hypotheses in action.
为那些假说提供了首个直接证据。
For a few years now, scientists have suspected that oxidative stress might speed up aging and certain diseases.
几年来，科学家们一直怀疑氧化应激可能加速衰老和某些疾病。
Now, this isn't psychological stress we're talking about.
现在这项研究所说的不是我们正在谈论的心理应激。
It's a chemical type of stress caused by internal factors like inflammation and obesity
是应激的一种化学类型，由一些内在因素引起，如炎症和肥胖
or external factors like exposure to pollution or cigarette smoke.
或外部因素，如暴露在污染或香烟烟雾中。
However it happens, it ultimately ends up creating free radicals: chemicals that can damage DNA, among other things.
但无论哪种情况，最终都会产生自由基：可以破坏DNA的化学物质。
Now, previous studies in human tissue have shown that oxidative stress can affect a part of your chromosomes called telomeres,
之前关于人体组织的研究表明氧化应激可以影响染色体中被称为端粒的部分，
which are caps that protect the free ends of the DNA strand kinda like the aglet at the end of your shoelace.
端粒是保护DNA链自由端的盖子，有点像是鞋带的末端的金属箍。
And now you know both what a telomere is and what an aglet is!
现在你就知道端粒和金属箍是什么啦！
Unlike with shoelaces, though, free DNA ends can end up stuck together in cells,
和鞋带不同，自由DNA末端最后会被困在细胞中，
and that prevents the chromosomes from separating properly during cell division.
阻止染色体在细胞分裂过程中正确分离。
Without telomeres, the whole genome can just turn into spaghetti.
没有了端粒，整个基因组就会变成意大利面条。
Here's the catch: every time the cell divides, your telomeres get shorter.
关键是，细胞每次分裂，你的端粒就会变得更短。
No matter how healthy your cells are, eventually the telomeres get so short that they stop replicating,
不论你的细胞有多么健康，最终端粒就会短到停止复制，
leaving behind a cell that is unable to divide.
最终剩下一个无法分裂的细胞。
And researchers think that leads to your organs basically aging.
研究人员认为这会导致器官衰老。
On the other hand, cancer cells are really good at maintaining their telomeres,
另一方面，癌细胞真的很擅长保养它们的端粒，
which is why they can grow and replicate indefinitely.
所以它们可以无限生长复制。
And whether it was a normal cell or cancerous, some of those previous models held
不论是正常细胞还是癌细胞，之前一些模型认为
that oxidative stress could basically enable spaghetti mode by interfering with telomere replication,
氧化应激通过干扰端粒复制，干扰细胞复制能力
thus interfering with the cell's ability to replicate and regulate its own lifespan.
并调剂寿命的方式促成意面模式。
But researchers couldn't test this in the past
但以前的科学家无法对此进行试验
because they didn't have a way of damaging just the telomeres without damaging the rest of the chromosome.
因为他们没有只破坏端粒而不损坏其余染色体的方法。
This new study came up with a tool to do exactly that.
这项新研究中提出的一种工具恰好可以做到。
They used a specific type of lesion called 8-oxoG,
他们利用一种被称为8-oxoG病变类型，
a common type of oxidative damage that replaces guanine, one of DNA's four A-T-C-G bases.
一种氧化性损伤常见类型，可以替代鸟嘌呤—DNA的四个A-T-C-G成分之一。
But they still had to localize this damage to the telomeres,
但他们仍需要对端粒的损伤进行定位，
so they used certain cancer cells with longer tips to test out their new mechanism.
所以他们使用了一些尖端较长的癌细胞来测试他们的新机制。
And they needed to be able to zap these things quickly and accurately.
他们需要能够快速准确地摧毁这些东西。
So they tagged one of the proteins around the telomere with a light activated molecule,
因此他们用一种光激活分子和一种荧光蛋白给端粒周围的一个蛋白质做上标记，
as well as a fluorescent protein so they could see the action a little more clearly.
这样他们就可以更清楚看到这些行动。
When just those ingredients existed together, nothing noteworthy happened.
当那些材料共存时，没有什么值得注意的事发生。
But when researchers excited the cells with a specific type of red light, they produced a free radical directly on the telomere.
但当研究人员用某种特殊红光刺激细胞时，它们直接在端粒上产生了一种自由基。
And this biological sniper shot worked, they created 8-oxoG lesions right where they wanted them.
这种生物狙击成功了，它们在所想之地创造出了8-oxoG损伤。
How did they know? Well, the researchers knew that certain cells have an enzyme that can actually remove 8-oxoG.
他们怎么知道的？研究人员知道某种携带酶的细胞可以移除8-oxoG。
It's a good defense to have for such a common problem.
对于这种常见问题，这是一个很好的防御。
By detecting that enzyme, the researchers confirmed the presence of oxidative damage.
通过检测这种酶，研究人员确认了氧化损伤的存在。
Sure enough, their new method caused the enzyme to show up specifically at the telomeres, confirming their hypothesis.
果然，他们的新方法让酶现身端粒，确认了他们的假设。
They repeated the process with a different line of cancer cells, and it worked similarly.
他们用另一种癌细胞重复了这一过程，同样也成功了。
Now knowing that their oxidative sniper worked, they started testing it out.
现在知道他们的氧化狙击器起作用了，他们开始进行测试。
They found that when they zapped the cells for a short amount of time,
他们发现当他们对细胞进行短时间的摧毁时，
there was some damage but otherwise healthy cells could repair themselves.
出现了一些损伤，但健康的细胞可以自我修复。
But when they did the same thing to cells without that defensive enzyme, they did see fragile telomeres,
但当他们对没有防御酶的细胞进行同样工作时，他们确实看到了脆弱的端粒
but with no real effect on cell growth. These first trials were faster, one-off exposures.
但对细胞生长没有实际影响。这些最初的试验更快，且是一次性曝光。
But when the researchers exposed the cells to the dye and light over the course of 24 days,
但当研究人员模拟长期氧化应激，将细胞暴露于染料
mimicking long term oxidative stress, they saw consistently shorter telomeres.
和光下超过24天后，他们看到始终都能看到更短的端粒。
And in that chronic exposure group, they saw that chromosomes with shortened telomeres went spaghetti mode
在慢性暴露组中，他们看到端粒缩短的染色体呈意大利面条状
and started fusing together, which affected their ability to make copies of themselves.
并开始融合在一起，这影响了它们自我复制的能力。
Now, all of this is a big deal, not just because the technology is new and cool, but because of the implications for studying disease.
这一切都非常重要，不仅是因为这项科技很新潮，还是因为研究疾病的意义。
In the study, cancer cells were able to recover from a single round of oxidative stress.
在研究中，癌细胞能够从单一轮氧化应激中恢复过来。
But when they exposed cells to it over time, they were more likely to stop replicating,
但随着时间推移，当他们将细胞暴露于其中时，它们更有可能停止复制，
which enhances our understanding of how oxidative stress relates to cancer development.
这增进了我们对氧化应激与癌症发展关联的理解。
Plus, understanding how oxidative stress works will help us understand its involvement in cellular aging or Alzheimers.
再加上，理解氧化应激如何起作用将帮助我们理解其在细胞衰老或阿尔茨海默症中起到的作用。
So while this study confirmed our suspicions about one model of oxidative stress, it opened many routes for further studies.
所以当这项研究确认我们对一种氧化应激模型的怀疑时，这为进一步研究敞开很多大门。
Thanks for watching this episode of SciShow News, and thanks to our President of Space Matthew Brant!
感谢收看本期《科学秀》，感谢Space的老板Matthew Brant！
If you'd like a shot at that title, or just want to join our amazing community of supporters, check out patreon.com/scishow.
如果你想试试那个头衔，或想加入社区成为我们的支持者的话，请登录patreon.com/scishow。
