Senile hair graying: H2O2‐mediated oxidative stress affects human hair color by blunting methionine sulfoxide repair

  title={Senile hair graying: H2O2‐mediated oxidative stress affects human hair color by blunting methionine sulfoxide repair},
  author={John M. Wood and Heinz Decker and H. Hartmann and Bhaven Chavan and Hartmut Rokos and Jennifer D. Spencer and Sybille Hasse and M. J. Thornton and Mohamed Shalbaf and Ralf Paus and K U Schallreuter},
  journal={The FASEB Journal},
  pages={2065 - 2075}
Senile graying of human hair has been the subject of intense research since ancient times. Reactive oxygen species have been implicated in hair follicle melanocyte apoptosis and DNA damage. Here we show for the first time by FT‐Raman spectroscopy in vivo that human gray/white scalp hair shafts accumulate hydrogen peroxide (H2O2) in millimolar concentrations. Moreover, we demonstrate almost absent catalase and methionine sulfoxide reductase A and B protein expression via immunofluorescence and… 
Age-Induced Hair Graying and Oxidative Stress
Age-induced hair graying (canities), or the age-induced loss of melanin synthesis and deposition within the hair shafts, is a noticeable and undesired sign of the aging process. Numerous mechanisms
Age‐induced hair greying – the multiple effects of oxidative stress
  • M. Seiberg
  • Biology
    International journal of cosmetic science
  • 2013
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.
Premature Graying as a Consequence of Compromised Antioxidant Activity in Hair Bulb Melanocytes and Their Precursors
Intricate coordinated mechanisms that govern the synchrony of hair growth and melanin synthesis remain largely unclear. These two events can be uncoupled in prematurely gray hair, probably due to
  • A. A.
  • Biology
    International Journal of Research -GRANTHAALAYAH
  • 2018
A new paradigm is herein introduced where the human hair medulla is excluded from H2O2 breakdown, thus inferring the absence of metabolic activity from FM.
The redox – biochemistry of human hair pigmentation
The effect of H2O2‐redox homeostasis on hair follicle pigmentation via tyrosinase, its substrate supply and signal transduction as well as the role of methionine sulfoxide repair via methionin sulfoxide reductases A and B (MSRA and B).
Stress-sensing in the human greying hair follicle: Ataxia Telangiectasia Mutated (ATM) depletion in hair bulb melanocytes in canities-prone scalp
The in vitro model of primary human scalp hair follicle melanocytes showed that ATM expression increased after incubation with the pro-oxidant hydrogen peroxide (H2O2), and the inhibition of ATM expression by chemical inhibition promoted the loss of melanocyte viability induced by oxidative stress.
Global Repigmentation Strategy of Grey Hair Follicles by Targeting Oxidative Stress and Stem Cells Protection
This active ingredient is developed which is capable of restoring all the disrupted mechanisms and of providing hair repigmentation within only 4 months, clearly evidenced that oxidative stress is a key factor in triggering a cascade of events leading to a loss of hair pigmentation.
The biology of human hair greying
It is emphasized that human greying invariably begins with the gradual decline in melanogenesis, including reduced tyrosinase activity, defective melanosome transfer and apoptosis of HFPU melanocytes, and is thus a primary event of the anagen hair bulb, not the bulge.
Blunted epidermal L‐tryptophan metabolism in vitiligo affects immune response and ROS scavenging by Fenton chemistry, part 1: epidermal H2O2/ONOO–‐mediated stress abrogates tryptophan hydroxylase and dopa decarboxylase activities, leading to low serotonin and melatonin levels
The data point to depletion of epidermal Trp by Fenton chemistry and exclude melatonin as a relevant contributor to epidersmal redox balance and immune response in vitiligo.
Human Hair Graying is Naturally Reversible and Linked to Stress
This work develops an approach to quantitatively profile natural graying events and their associated proteomic signatures along individual human hairs, resulting in a quantifiable physical timescale of aging and provides a new model to examine the modifiability of human aging.


Towards a “free radical theory of graying”: melanocyte apoptosis in the aging human hair follicle is an indicator of oxidative stress induced tissue damage
It is concluded that oxidative stress is high in hair follicle melanocytes and leads to their selective premature aging and apoptosis and the graying hair follicles offers a unique model system to study oxidative stress and aging.
Identification of epidermal L‐tryptophan and its oxidation products by in vivo FT‐Raman Spectroscopy further supports oxidative stress in patients with vitiligo
In the past, non-invasive in vivo FT-Raman spectroscopy has been used to detect H2O2-mediated oxidation of methionine to methionine sulfoxide and methionine sulfone, as well as cysteine to cysteic
Increased melanocyte apoptosis under stress-mediator Substance P – elucidating pathways involved in stress-induced premature graying
The results suggest a precocious exhaustion of the melanocyte stem cell pool due to an enhanced turnover of pigment cell precursors as a pathway involved in premature canities.
Oxidative stress via hydrogen peroxide affects proopiomelanocortin peptides directly in the epidermis of patients with vitiligo.
H2O2-mediated oxidation of epidermal ACTH, alpha-MSH, and beta-endorphin in vitiligo owing to oxidation of methionine residues in the sequences of these peptides is demonstrated.
The repair enzyme peptide methionine-S-sulfoxide reductase is expressed in human epidermis and upregulated by UVA radiation.
The expression of human methionine sulfoxide reductase A (MSRA) was investigated in HaCaT cells, primary human keratinocytes, and in human skin to assess the functional relevance of the enzyme and its expression in response to UVB, UVA, and H(2)O(2).
Low catalase levels in the epidermis of patients with vitiligo.
A new hypothesis has been formulated for the pathogenesis of vitiligo based on a consistent reduction in levels of catalase compared to normal healthy controls of matched photo-skin types and a increase in the concentration of hydrogen peroxide in the epidermis of these patients.
Functioning methionine sulfoxide reductases A and B are present in human epidermal melanocytes in the cytosol and in the nucleus.
Methionine sulfoxide reductases A and B are deactivated by hydrogen peroxide (H2O2) in the epidermis of patients with vitiligo.
It is shown that the expression/activities of MSRA and MSRB are significantly decreased in the epidermis of patients with vitiligo compared to healthy controls and this results confirm that very important anti-oxidant enzymes are seriously affected in acute Vitiligo.