spontaneous DNA damage (depurination and deamination)

DNA is often pictured as a stable archive, but at body temperature, sitting in water, it is slowly falling apart on its own — no radiation, no chemicals required. Ordinary thermal jostling and the simple presence of the watery cell are enough to chip away at its chemistry. This unprompted decay is called spontaneous DNA damage, and two of its most frequent forms are depurination and deamination.

Depurination is the loss of a base from the backbone: the bond holding a purine (A or G) to the sugar quietly breaks by reaction with water, leaving a gap with no base — an abasic site — while the backbone stays intact. A single human cell loses on the order of thousands of purines a day this way. Deamination is the loss of an amino group from a base; the classic case is cytosine turning into uracil. This matters enormously, because uracil pairs like thymine, so an unrepaired deaminated cytosine reads as a T in the next round of copying — a C-to-T mutation waiting to happen.

The honest picture is that the genome is under constant, low-level chemical assault from inside, every cell, every day, just from being a wet molecule at 37 degrees. The reason this does not melt our genes into noise is that repair systems are tirelessly fixing it: base excision repair is built precisely to pluck out uracil and patch abasic sites. Spontaneous damage is also why cytosine deamination is such a hotspot for mutation, and why the rare base 5-methylcytosine — which deaminates to thymine, a normal base that is harder to flag as wrong — is a notorious mutational weak point in our DNA.