Graying hair could be a sign that the body is effectively protecting itself from cancer, suggests a new study conducted by researchers from the University of Tokyo and published in the journal Nature Cell Biology, reports Live Science, taken over by Agerpres.
Cancer-causing triggers, such as ultraviolet (UV) light or certain chemicals, activate a natural defense pathway that leads to premature bleaching but reduces the incidence of cancer, research shows.
Gray hair is a response to DNA damage
Japanese researchers tracked down the stem cells responsible for producing the pigment that gives hair color. In experiments on mice, they found that these cells responded to DNA damage either by stopping growth and division – leading to gray hair – or by replicating out of control to form a tumor.
The study highlights the importance of these types of protective mechanisms that emerge with age as a defense against DNA damage and disease, according to the study authors.
Healthy hair growth depends on a constantly renewing population of stem cells in the hair follicle. A small pocket in the follicle contains reserves of melanocyte stem cells (McSCs) – precursors to the cells that produce the melanin pigment that gives hair color.
“At each cycle of hair regeneration, these melanocyte stem cells will divide and produce mature, differentiated cells,” said Dot Bennett, a cell biologist at City St George's, University of London, who was not involved in the study. “They migrate into the hair follicle and start producing pigment.”
Graying occurs when these cells can no longer produce enough pigment to properly color each strand. “It's a kind of exhaustion called cellular senescence,” Bennett explained. “It is a limit to the total number of divisions a cell can go through and appears to be an anti-cancer mechanism to prevent the uncontrolled propagation of random genetic errors acquired over time.”
When the melanocyte stem cells reach this point, they stop dividing, which means that the follicle no longer has a source of pigment to color the hair. This usually happens with old age, as stem cells naturally reach this limit.
However, Emi Nishimura, a professor of stem cell aging medicine and co-leader of the study with colleagues at the University of Tokyo, said they were interested in how the same mechanism works in response to DNA damage – a key trigger for cancer development.
The role of melanocyte stem cells
In the mouse studies, the team used a combination of techniques to track individual melanocyte stem cells' progress through the hair cycle after exposing them to various harmful environmental conditions, including ionizing radiation and carcinogenic compounds. They observed that the type of damage influenced the way the cells reacted.
Thus, ionizing radiation determined the differentiation and maturation of stem cells and, finally, activated the biochemical pathway responsible for cellular senescence. As a result, the reserves of melanocyte stem cells are quickly depleted during the hair cycle, thus stopping the production of mature pigment cells and leading to graying.
Meanwhile, by essentially stopping cell division, this senescence pathway prevented the mutated DNA from being passed on to a new generation of cells, making it less likely that these cells would form cancerous tumors.
Exposure to chemical carcinogens—such as 7,12-dimethylbenzanthracene (DMBA), a tumor initiator widely used in cancer research—appears to bypass this protective mechanism, blocking cellular senescence in mouse studies and allowing hair follicles to retain their stem cell reserves and ability to produce pigment, even after DNA damage. Thus the hair kept its color, but in the long term, the uncontrolled replication of the damaged DNA led to the formation of tumors and cancer, the team said in a statement.
The next step will be to replicate the results obtained on mouse hair on human hair follicles, to verify the validity of these observations.
