F1 THE AGING HAIR FOLLICLE DISPLAYS OXIDATIVE STRESS ASSOCIATED MELANOCYTE-LOSS BUT DOES NOT LOOSE ITS CAPACITY TO GROW: A MODEL FOR TISSUE SPECIFIC AGING
Overall R1, Handjiski B1, Birch-Machin M2, Spatz K1, Klapp BF1, Arck PC1, Peters EMJ1
1Psychoneuroimmunology, Department of Internal Medicine, Psychosomatics, University-Medicine Charité, Campus Virchow, Humboldt-University of Berlin, Germany
2Dermatological Sciences, School of Clinical and Laboratory Sciences, The Medical School, University of Newcastle, Newcastle upon Tyne, United Kingdom

Psychoemotional stress can lead to increased oxidative and inflammatory stress both of which have been associated with the aging process. One prominent sign of aging, the graying of hair, is an intriguing, much discussed phenomenon in this context. Interestingly, the continuous melanin synthesis in the growing (anagen) hair follicle generates high levels of free radicals selectively in hair bulb melanocytes. We therefore hypothesize, that high endogenous oxidative stress renders hair bulb melanocytes highly susceptible to additional stressors and subsequent premature aging. To test this hypothesis, we dissected human scalp skin anagen hair follicles from graying individuals and subjected them to macroscopic and immunohistomorphometric analysis and organ culture experiments. We found evidence of increased oxidative stress and melanocyte apoptosis in the pigmentary-unit of hair follicles from graying individuals. By PCR, the `common´ deletion, a marker mitochondrial DNA-deletion for accumulating oxidative stress damage, most prominently occurred in isolated graying hair follicles. Cultured pigmented hair follicles exposed to exogenous oxidative stress (hydroquinone) showed increased melanocyte apoptosis in the hair bulb. However, unpigmented hair follicles showed better hair growth in culture, than pigmented hair follicles of the same donor. We conclude that oxidative stress is high in the hair follicle melanocyte and that this leads to the selective premature damage and apoptosis of this cell population. This process may be triggered and hastened by exogenous oxidative stress for example during psychoemotional stress and inflammation. Antioxidants and protection from additional oxidative stress should proof a useful measure to slow down this process.