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Scientists have had a variety of hypotheses about how chemical stress can affect DNA to cause aging, but a new study has just shown the process in action.

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[INTRO ♪].

Over the last few decades, scientists have described some hypotheses explaining how stress can accelerate aging. And a new study published in Molecular Cell this week from the University of Pittsburgh provided the first direct evidence of one of those hypotheses in action.

For a few years now, scientists have suspected that oxidative stress might speed up aging and certain diseases. Now, this isn't psychological stress we're talking about. It's a chemical type of stress caused by internal factors like inflammation and obesity or external factors like exposure to pollution or cigarette smoke.

However it happens, it ultimately ends up creating free radicals: chemicals that can damage DNA, among other things. Now, previous studies in human tissue have shown that oxidative stress can affect a part of your chromosomes called telomeres, which are caps that protect the free ends of the DNA strand kinda like the aglet at the end of your shoelace. And now you know both what a telomere is and what an aglet is!

Unlike with shoelaces, though, free DNA ends can end up stuck together in cells, and that prevents the chromosomes from separating properly during cell division. Without telomeres, the whole genome can just turn into spaghetti. Here's the catch: every time the cell divides, your telomeres get shorter.

No matter how healthy your cells are, eventually the telomeres get so short that they stop replicating, leaving behind a cell that is unable to divide. And researchers think that leads to your organs basically aging. On the other hand, cancer cells are really good at maintaining their telomeres, which is why they can grow and replicate indefinitely.

And whether it was a normal cell or cancerous, some of those previous models held that oxidative stress could basically enable spaghetti mode by interfering with telomere replication, thus interfering with the cell's ability to replicate and regulate its own lifespan. But researchers couldn't test this in the past because they didn't have a way of damaging just the telomeres without damaging the rest of the chromosome. This new study came up with a tool to do exactly that.

They used a specific type of lesion called 8-oxoG, a common type of oxidative damage that replaces guanine, one of DNA's four A-T-C-G bases. But they still had to localize this damage to the telomeres, so they used certain cancer cells with longer tips to test out their new mechanism. And they needed to be able to zap these things quickly and accurately.

So they tagged one of the proteins around the telomere with a light activated molecule, as well as a fluorescent protein so they could see the action a little more clearly. When just those ingredients existed together, nothing noteworthy happened. But when researchers excited the cells with a specific type of red light, they produced a free radical directly on the telomere.

And this biological sniper shot worked—they created 8-oxoG lesions right where they wanted them. How did they know? Well, the researchers knew that certain cells have an enzyme that can actually remove 8-oxoG.

It's a good defense to have for such a common problem. By detecting that enzyme, the researchers confirmed the presence of oxidative damage. Sure enough, their new method caused the enzyme to show up specifically at the telomeres, confirming their hypothesis.

They repeated the process with a different line of cancer cells, and it worked similarly. Now knowing that their oxidative sniper worked, they started testing it out. They found that when they zapped the cells for a short amount of time, there was some damage but otherwise healthy cells could repair themselves.

But when they did the same thing to cells without that defensive enzyme, they did see fragile telomeres, but with no real effect on cell growth. These first trials were faster, one-off exposures. But when the researchers exposed the cells to the dye and light over the course of 24 days, mimicking long term oxidative stress, they saw consistently shorter telomeres.

And in that chronic exposure group, they saw that chromosomes with shortened telomeres went spaghetti mode and started fusing together, which affected their ability to make copies of themselves. 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. In the study, cancer cells were able to recover from a single round of oxidative stress.

But when they exposed cells to it over time, they were more likely to stop replicating, which enhances our understanding of how oxidative stress relates to cancer development. Plus, understanding how oxidative stress works will help us understand its involvement in cellular aging or Alzheimers. So while this study confirmed our suspicions about one model of oxidative stress, it opened many routes for further studies.

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