Cited by 94melanin and skin pigmentationHair Growth and DisordersMelanoma and MAPK Pathways

Age-induced hair greying – the multiple effects of oxidative stress

Seiberg, M.·2013·International Journal of Cosmetic Science

Abstract

An obvious sign of ageing is hair greying, or the loss of pigment production and deposition within the hair shafts. Numerous mechanisms, acting at different levels and follicular locations, contribute to hair greying, ranging from melanocyte stem cells defects to follicular melanocyte death. One key issue that is in common to these processes is oxidative damage. At the hair follicle stem cells niche, oxidative stress, accelerated by B-cell lymphoma 2 gene (BCL-2) depletion, leads to selective apoptosis and diminution of melanocyte stem cells, reducing the repopulation of newly formed anagen follicles. Melanotic bulbar melanocytes express high levels of BCL-2 to enable survival from melanogenesis- and ultraviolet A (UVA)-induced reactive oxygen species (ROS) attacks. With ageing, the bulbar melanocyte expression of anti-oxidant proteins such as BCL-2, and possibly TRP-2, is reduced, and the dedicated enzymatic anti-oxidant defence system throughout the follicle weakens, resulting in enhanced oxidative stress. A marked reduction in catalase expression and activity results in millimolar accumulation of hydrogen peroxide, contributing to bulbar melanocyte malfunction and death. Interestingly, amelanotic melanocytes at the outer root sheath (ORS) are somewhat less affected by these processes and survive for longer time even within the white, ageing hair follicles. Better understanding of the overtime susceptibility of melanocytes to oxidative stress at the different follicular locations might yield clues to possible therapies for the prevention and reversal of hair greying.

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Crossref · 10.1111/ics.12090

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  • Aging-associated hair greying involves loss of melanocyte stem cells by PCD.

    “Aging-associated hair greying involves loss of melanocyte stem cells by PCD, and decreased Bcl-2 and increased ROS are implicated in this process (Seiberg, 2013).”

    From Programmed cell death in aging (2015) · cites this paper as Seiberg, 2013

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Authors
Seiberg, M.
Affiliations
Seiberg Consulting LLC Princeton NJ USA
Corresponding author
Seiberg, M.
Venue
International Journal of Cosmetic Science
Publisher
Wiley
Published
2013-10-10
Volume
35
Issue
6
Pages
532-538
ISSN
  • 0142-5463 (ISSN-L)
  • 1468-2494
OpenAlex
W2072811763
Cited by
94
References
87
Citations by year
2026: 11 · 2025: 8 · 2024: 10 · 2023: 10 · 2022: 7 · 2021: 5 · 2020: 10 · 2019: 9 · 2018: 6 · 2017: 4 · 2016: 4 · 2015: 7 · 2014: 3
FWCI
0.54
Type
journal article
Language
en
Open access
closed
Locations
  • International Journal of Cosmetic Science (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › melanin and skin pigmentation
  • Health Sciences › Medicine › Urology › Hair Growth and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
Keywords
hair graying, aging, oxidative stress, melanocytes, melanocyte stem cells, Bcl-2, apoptosis, reactive oxygen species, catalase, hydrogen peroxide, melanogenesis, outer root sheath, hair follicle, TRP-2, hair pigmentation
MeSH terms
Aging, Hair Color, Humans, Melanins, Melanocytes, Reactive Oxygen Species, Hair Follicle, Genes, bcl-2, Intramolecular Oxidoreductases, PTEN Phosphohydrolase

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