Every month OUP editor and author Jonathan Crowe answers your science questions in the monthly SciWhys column. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can.
Today: how do cells age?
By Jonathan Crowe
We’ve all been there: the car that finally became too expensive to keep on the road as more and more parts needed to be replaced, or the computer that started to run so slowly you gave up even bothering to open your web browser. These and other everyday experiences show how there’s an increased risk of things breaking as they get older. And our own bodies aren’t immune: the hair at my temples (and on other parts of my head, I fear) is on a resolute march towards greyness, and my eyesight isn’t as sharp as it once was. In short, our cells are just as susceptible to breaking down as they age as anything else.
But what causes a cell to age? In part, at least, it seems to be owing to cells accumulating damage as time passes. And if it’s our genome – the instruction manual for our survival – that is damaged, real problems can ensue (as we’ll see later in this post). So how does this damage arise? For a start, our surroundings can be a real threat. For example, we’re all advised not to spend a lot of time exposing our skin to intense sunlight. Why? Because the same ultra-violet rays in sunlight (and sunbeds) that give us a tan can also damage our DNA, changing the information it carries. (The biological information carried by skin cells is most at risk of being affected because skin cells are most heavily exposed to sunlight.)
Even oxygen, which we must continually inhale if we’re to survive, has a nasty sting in its tail. Once it enters the body, oxygen can undergo chemical change to become what is called a reactive oxygen species – a nasty piece of work that can do serious damage to substances that it bumps into, including our information-carrying genome. It’s a real double-edged sword: we must breathe in oxygen to survive, yet it can also do a lot of damage once inside us.
Even the process of a cell dividing has its risks. Every time a cell divides it has to copy its genome so that each of its daughter cells contains all of the biological information it needs to survive. But every time a copy of the genome is made, there’s a risk of errors creeping in. Imagine copying this blog post 1000 times, with one error creeping in each time. If you were to read the first few copies the words on the page would still make sense, despite the occasional error. But, by the one-thousandth copy, the multitude of errors would probably render the words all but unintelligible. And the same is true of genomes: as more and more copies are made, more errors are likely to creep in, corrupting the information that genome originally contained.
So why are these errors – however generated – such a problem? In short, because the growth of cells has to be carefully controlled, but it’s difficult to maintain this control in a damaged cell. Why is this? I described in a previous post how our genome is like a library, with information held in ‘books’ called chromosomes, and with these chromosomes split into chapters called genes. Some of these chapters – these genes – contain instructions for regulating the growth of cells. If these instructions are corrupted because of errors introduced when the library of information is copied, the cell can no longer make sense of them, and the regulation these instructions enabled will be lost. (It’s a bit like having a brake to control the speed of a car; if the brake ceases to work, the speed of the car becomes much more difficult to regulate.)
One consequence of being unable to ‘apply the brakes’ to cell division is the formation of a tumour, which many of us will recognise as a hallmark of cancer. A tumour forms when a cell starts to grow in an uncontrolled way, dividing time and time again without pause to form a mass of daughter cells – the tumour itself.
So how can our bodies avoid the risk of their cells carrying faulty information? The answer: they don’t let cells get too old. To reduce the risk of damage accumulating, cells only divide a certain number of times before being retired from service. Essentially, cells are eliminated before they get so old that they run the risk of becoming dangerous.
But how do cells know how many times they have divided? Cunningly, cells have a built-in counter – a special segment at each end of every chromosome (called a ‘telomere’), which acts as a measuring device. Each time a cell replicates, a little bit is nibbled away from the end of each of its chromosomes causing the telomere to shrink slightly. Over time, as the cell divides again and again, the telomeres shorten to the point at which they get too short; at this point, the counter essentially reaches zero, and the cell can no longer divide.
Despite best intentions (and ingenious control mechanisms) things do go wrong. In some cancer cells the ends of chromosomes are constantly repaired instead of being nibbled away bit by bit. This means the telomeres never get shorter, and the cell counter fails to count down to zero. As a result, the cells continue to grow unchecked, leading to the spectre of tumour formation.
For much of the time, though, an amazing balancing act is successfully achieved, with new cells continually being created and old cells being retired to maintain the status quo. In fact, we find ourselves in a new skin every month (whether we realise it or not) as old skin cells are retired and new ones replace them. That’s quite a feat of self-preservation.
Jonathan Crowe is Editor in Chief for Natural, Health & Clinical Sciences in the Higher Education Department at Oxford University Press. A biochemistry graduate, he manages OUP’s undergraduate textbook publishing programme across a range of science and science-related disciplines. He is also an author of Chemistry for the Biosciences, now in its second edition, and was a runner-up in the Daily Telegraph/BASF Young Science Writer Awards (in 2001, when he was still classed as being ‘young’). You can read more about OUP’s science books here.