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Oxidative Stress in Ageing of Hair

Experimental evidence supports the hypothesis that oxidative stress plays a major role in the ageing process. Reactive oxygen species are generated by a multitude of endogenous and environmental challenges. Reactive oxygen species or free radicals are highly reactive molecules that can directly dama...

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Detalles Bibliográficos
Autor principal: Trüeb, Ralph M
Formato: Texto
Lenguaje:English
Publicado: Medknow Publications 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929555/
https://www.ncbi.nlm.nih.gov/pubmed/20805969
http://dx.doi.org/10.4103/0974-7753.51923
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author Trüeb, Ralph M
author_facet Trüeb, Ralph M
author_sort Trüeb, Ralph M
collection PubMed
description Experimental evidence supports the hypothesis that oxidative stress plays a major role in the ageing process. Reactive oxygen species are generated by a multitude of endogenous and environmental challenges. Reactive oxygen species or free radicals are highly reactive molecules that can directly damage cellular structural membranes, lipids, proteins, and DNA. The body possesses endogenous defence mechanisms, such as antioxidative enzymes and non-enzymatic antioxidative molecules, protecting it from free radicals by reducing and neutralizing them. With age, the production of free radicals increases, while the endogenous defence mechanisms decrease. This imbalance leads to the progressive damage of cellular structures, presumably resulting in the ageing phenotype. Ageing of hair manifests as decrease of melanocyte function or graying, and decrease in hair production or alopecia. There is circumstantial evidence that oxidative stress may be a pivotal mechanism contributing to hair graying and hair loss. New insights into the role and prevention of oxidative stress could open new strategies for intervention and reversal of the hair graying process and age-dependent alopecia.
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spelling pubmed-29295552010-08-30 Oxidative Stress in Ageing of Hair Trüeb, Ralph M Int J Trichology Review Article Experimental evidence supports the hypothesis that oxidative stress plays a major role in the ageing process. Reactive oxygen species are generated by a multitude of endogenous and environmental challenges. Reactive oxygen species or free radicals are highly reactive molecules that can directly damage cellular structural membranes, lipids, proteins, and DNA. The body possesses endogenous defence mechanisms, such as antioxidative enzymes and non-enzymatic antioxidative molecules, protecting it from free radicals by reducing and neutralizing them. With age, the production of free radicals increases, while the endogenous defence mechanisms decrease. This imbalance leads to the progressive damage of cellular structures, presumably resulting in the ageing phenotype. Ageing of hair manifests as decrease of melanocyte function or graying, and decrease in hair production or alopecia. There is circumstantial evidence that oxidative stress may be a pivotal mechanism contributing to hair graying and hair loss. New insights into the role and prevention of oxidative stress could open new strategies for intervention and reversal of the hair graying process and age-dependent alopecia. Medknow Publications 2009 /pmc/articles/PMC2929555/ /pubmed/20805969 http://dx.doi.org/10.4103/0974-7753.51923 Text en © International Journal of Trichology http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Trüeb, Ralph M
Oxidative Stress in Ageing of Hair
title Oxidative Stress in Ageing of Hair
title_full Oxidative Stress in Ageing of Hair
title_fullStr Oxidative Stress in Ageing of Hair
title_full_unstemmed Oxidative Stress in Ageing of Hair
title_short Oxidative Stress in Ageing of Hair
title_sort oxidative stress in ageing of hair
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929555/
https://www.ncbi.nlm.nih.gov/pubmed/20805969
http://dx.doi.org/10.4103/0974-7753.51923
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