When an aging mouse's lovely brown fur turns grey, she can now officially blame stress — at least, the kind of stress that damages DNA, Japanese researchers have confirmed.

Using experiments on mice, Ken Inomata of Kanazawa University, Emi Nishimura of Tokyo Medical and Dental University and their colleagues teased out the apparent mechanism that causes hair to lose its colour during aging. Their results are published in Friday's issue of the journal Cell.

The researchers subjected mice to high levels of a type of stress called "genotoxic stress," which damages DNA — something that all living organisms experience constantly through exposure to ultraviolet light, other radiation and certain types of chemicals.

""It is estimated that a single cell in mammals can encounter approximately 100,000 DNA damaging events per day," Nishimura said.

Cells have ways to repair themselves, but can be damaged irreversibly by excessive stress.

In the experiment, heavy stress was caused by exposing the mice to x-rays or injecting them with DNA-damaging chemicals such as hydrogen peroxide. The researchers then carefully observed changes in the cells.

Hair follicles contain stem cells, relatively unspecialized cells that can mature into more specialized cells. Those stem cells are responsible for making pigment-producing cells called melanocytes. While the stem cells reproduce periodically, the melanocytes don't and eventually die.

Stress makes stem cells mature: study

The researchers found that when the stem cells were damaged by genotoxic stress, they turned into mature melanocyte cells instead of remaining stem cells.

However, they remained in the area where stem cells are usually found — a place where melanocytes don't usually grow. In previous studies, other researchers had found it puzzling that melanocytes appeared in the wrong place as an organism ages.

Because melanocytes die without reproducing, the stem cell population will dwindle and hair will turn grey if too many stem cells turn into mature melanocytes. However, the researchers suggested that turning damaged stem cells into melanocytes might be needed to ensure the overall stem cell population is healthy and to prevent cancer.

The study also found that the normal version of a faulty gene involved in premature aging syndromes can protect stem cells from turning into adult pigment cells.

The results support the hypothesis that visible signs of aging may be caused by damage to long-lived stem cell populations, the paper said.