Can DNA damage in your cells repair itself?

Your cells are constantly and actively repairing DNA damage. Each of your cells has to deal with tens of thousands of instances of damage every day, caused by sunlight, metabolic by-products, and simply the wear and tear of life. Multiple repair mechanisms work in parallel to remove or bypass that damage, keeping the cell functioning.

The repair capacity is impressive, but it has limits. Single-strand damage is repaired relatively quickly and without errors. Double-strand breaks, where both strands of the DNA are severed at the same time, are the most dangerous. These take more time and are not always repaired perfectly. What remains can lead to small errors in the genetic code, or in more serious cases to instability of the entire hereditary material.

When those repair systems structurally fall short or become dysregulated, damage accumulates. This is one of the most important drivers of cancer: tumour cells are often characterised by precisely this kind of instability. Conversely, cancer cells can overdo their repair capacity, allowing them to quickly fix the damage inflicted by chemotherapy. This is a well-known mechanism behind therapy resistance, demonstrated in cell and animal models for cancers including breast and colorectal cancer.

Not all DNA in your body is equally well protected. The DNA in the mitochondria, the energy factories of your cells, is more accessible to damage than the DNA in the cell nucleus, and the repair mechanisms there are less well understood. Damage to mitochondrial DNA has been linked to multiple diseases, but exactly how that repair works is still very much the subject of ongoing research.

A more specialised example: in the ovaries, disrupted DNA repair mechanisms in certain supporting cells may contribute to premature ovarian failure. This has so far only been observed in laboratory and mouse models, so no clinical applications have yet emerged from it.