Towards a "free radical theory of graying"
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Towards a "free radical theory of graying" : melanocyte apoptosis in the aging human hair follicle is an indicator of oxidative stress induced tissue damage. / Arck, Petra Clara; Overall, Rupert; Spatz, Katharina; Liezman, Christiane; Handjiski, Bori; Klapp, Burghard F; Birch-Machin, Mark A; Peters, Eva Milena Johanne.
In: FASEB J, Vol. 20, No. 9, 07.2006, p. 1567-9.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Towards a "free radical theory of graying"
T2 - melanocyte apoptosis in the aging human hair follicle is an indicator of oxidative stress induced tissue damage
AU - Arck, Petra Clara
AU - Overall, Rupert
AU - Spatz, Katharina
AU - Liezman, Christiane
AU - Handjiski, Bori
AU - Klapp, Burghard F
AU - Birch-Machin, Mark A
AU - Peters, Eva Milena Johanne
PY - 2006/7
Y1 - 2006/7
N2 - Oxidative stress is generated by a multitude of environmental and endogenous challenges such as radiation, inflammation, or psychoemotional stress. It also speeds the aging process. Graying is a prominent but little understood feature of aging. Intriguingly, the continuous melanin synthesis in the growing (anagen) hair follicle generates high oxidative stress. We therefore hypothesize that hair bulb melanocytes are especially susceptible to free radical-induced aging. To test this hypothesis, we subjected human scalp skin anagen hair follicles from graying individuals to macroscopic and immunohistomorphometric analysis and organ culture. We found evidence of melanocyte apoptosis and increased oxidative stress in the pigmentary unit of graying hair follicles. The "common" deletion, a marker mitochondrial DNA-deletion for accumulating oxidative stress damage, occurred most prominently in graying hair follicles. Cultured unpigmented hair follicles grew better than pigmented follicles of the same donors. Finally, cultured pigmented hair follicles exposed to exogenous oxidative stress (hydroquinone) showed increased melanocyte apoptosis in the hair bulb. We conclude that oxidative stress is high in hair follicle melanocytes and leads to their selective premature aging and apoptosis. The graying hair follicle, therefore, offers a unique model system to study oxidative stress and aging and to test antiaging therapeutics in their ability to slow down or even stop this process.
AB - Oxidative stress is generated by a multitude of environmental and endogenous challenges such as radiation, inflammation, or psychoemotional stress. It also speeds the aging process. Graying is a prominent but little understood feature of aging. Intriguingly, the continuous melanin synthesis in the growing (anagen) hair follicle generates high oxidative stress. We therefore hypothesize that hair bulb melanocytes are especially susceptible to free radical-induced aging. To test this hypothesis, we subjected human scalp skin anagen hair follicles from graying individuals to macroscopic and immunohistomorphometric analysis and organ culture. We found evidence of melanocyte apoptosis and increased oxidative stress in the pigmentary unit of graying hair follicles. The "common" deletion, a marker mitochondrial DNA-deletion for accumulating oxidative stress damage, occurred most prominently in graying hair follicles. Cultured unpigmented hair follicles grew better than pigmented follicles of the same donors. Finally, cultured pigmented hair follicles exposed to exogenous oxidative stress (hydroquinone) showed increased melanocyte apoptosis in the hair bulb. We conclude that oxidative stress is high in hair follicle melanocytes and leads to their selective premature aging and apoptosis. The graying hair follicle, therefore, offers a unique model system to study oxidative stress and aging and to test antiaging therapeutics in their ability to slow down or even stop this process.
KW - Aging/physiology
KW - Free Radicals
KW - Hair Color/physiology
KW - Hair Follicle/growth & development
KW - Humans
KW - Melanocytes/cytology
KW - Models, Biological
KW - Oxidative Stress/physiology
U2 - 10.1096/fj.05-4039fje
DO - 10.1096/fj.05-4039fje
M3 - SCORING: Journal article
C2 - 16723385
VL - 20
SP - 1567
EP - 1569
JO - FASEB J
JF - FASEB J
SN - 0892-6638
IS - 9
ER -