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Age-induced hair graying
A possible role for oxidative stress


Seiberg Consulting, LLC, Princeton NJ, USA


Hair graying, or the loss of pigment within hair shafts, is a hallmark of the aging process. Numerous mechanisms contribute to age-induced hair graying, affecting both melanocyte stem cells and follicular melanocytes. Many of these processes are induced, directly or indirectly, by oxidative damage. Melanocyte stem cells exposed to cumulative oxidative damage undergo apoptosis and therefore decrease the repopulation of fully differentiated follicular melanocytes. Bulbar melanocytes reduce the expression of anti-oxidant proteins upon aging, with a marked reduction in catalase expression and activity, resulting in melanocyte malfunction and death. Better understanding of the exposure and sensitivity of different melanocytes populations to oxidative stress might yield clues to possible interventions in the hair graying process.


Human hair has no significant biological role, and is kept, removed, styled or colored for cosmetic reasons only. Scalp hair loss and hair graying (canities) are visual consequence of the aging process, and are cosmetically undesired. Grey (British) or gray (American) hair color may make individuals look and feel older, and is of concern in our society, as expressed by the commonly believed (but inaccurate) “Rule of 50” (50% of 50 year-olds have about 50% gray hairs) (1).
Strategies to hide hair graying range from the use of natural preparations for hair coloring, which have been documented from about 1500 BC, to today’s hair colorants and chemical processes. Reversing hair graying is highly desired, however there is no scientific evidence that any diet, supplement, herbal remedy or product could slow, stop or reverse human hair graying. Regardless, many such agents are used by different societies with claimed effectiveness.
Mechanisms implicated in age-induced hair graying include the loss of melanocyte stem cells or their failure to differentiate, defects in melanocyte migration, anagen defects, melanocyte death, ...