Follicle oxidative stress
Follicular Oxidative Stress
Also searched as Follicular Oxidative Stress.
You want it lowered: easing follicular oxidative stress protects hair growth and color.
In depth
Follicular oxidative stress — the reactive-oxygen burden that ages the hair follicle and drives shedding and graying.
What drives it
Radiation exposure increases it.
Both sides of the question were opened. Verbatim: “The evidence for or against a relation between RF-EMF and biomarkers of oxidative stress is overall of very low certainty.”. PMID 39566441
Testosterone increases it.
Androgen/DPC-ROS study 2013, BMB Rep — dihydrotestosterone (androgen) increases reactive-oxygen-species generation in hair-follicle dermal papilla cells, mediating downstream TGF-β1 induction. PMC4133876
Antioxidant defense reduces it.
NRF2 is the master redox regulator expressed in the hair follicle and counters follicular oxidative stress. In detail: NRF2 is a CNC-bZIP transcription factor regulating the basal and inducible expression of a wide array of antioxidant genes; on dissociation from KEAP1 it accumulates in the nucleus and transactivates the antioxidant response element of NQO1, HMOX1, glutamate-cysteine ligase and the glutathione-S-transferases (PMC6259123; PMC3677633). Loss-of-function is decisive: mice with targeted disruption of the nrf2 gene ARE prone to develop lesions in response to environmental toxicants, carcinogens, drugs and inflammatory insults. ChIP-seq in mouse embryonic fibroblasts and human lymphoblastoid cells found several hundred NRF2 targets in processes other than oxidative stress — protein transport, phosphorylation, cell cycle, growth, adipogenesis, iron and heme metabolism. NRF2 is not a dedicated antioxidant switch. The caveat that must travel with every NRF2 claim: NRF2 activation is not uniformly good. Tumors carry activating NRF2 mutations, and NRF2 cancer target genes are functionally linked to metabolic, proliferative and chemoresistance advantages; glutathione and thioredoxin are described as essential for cancer initiation and progression (Redox Biol 2018, doi 10.1016/j.redox.2018.06.006). In SDHB-deficient tumor cells, NRF2-guided glutathione synthesis supports survival and proliferation, and NRF2 blockade caused severe cytotoxicity — the NRF2 inhibitor brusatol is being developed as a therapy. doi 10.1016/j.redox.2018.06.006 · PMC6259123
Heart muscle inflammation increases it.
The oxidative burden, and it moves with the dose. In the eam model, treatment 'induced a significant decrease of PROOXIDANTS production (O2⁻, H2O2, and TBARS) and improved antioxidant defense system via increase in GSH, SOD, and CAT... with medium and high dose being more effective than low dose' (pmc8901324 — Melissa officinalis l. Supplementation Provides Cardioprotection in a Rat Model of Experimental Autoimmune Myocarditis). ⇒ a redox shift alongside a recovery of pump function.
What it drives
It reduces Hair.
Trüeb 2009, Int J Trichology — follicular oxidative stress (ROS) drives dermal-papilla senescence and secretion of hair-growth inhibitors (TGF-β1/2), promoting androgenetic alopecia and graying. PMC2929555
It increases Reduces scarring.
Balding dermal papilla cells secreted higher levels of the negative hair growth regulators transforming growth factor beta 1 and 2 in response to H2O2. Replicated in independent work: HFDPCs from balding scalp ARE more vulnerable to oxidative stress, leading to enhanced secretion of TGF-beta, a well-established inhibitor of hair growth, and accelerated cellular senescence. The point: peroxide is not corroding the hair. It is making the papilla issue the shutdown order. That is why an antioxidant that reaches the papilla is a different proposition from one that does not and a specificity the first paper insists on: the TGF-beta rise occurred in response to H2O2 but not cell culture-associated oxidative stress. Not all oxidative stress is the same stimulus. doi 10.1038/JID.2015.28 · PMC12898851
It increases Hair pigment loss.
Melanogenesis is inherently a pro-oxidative biosynthetic pathway — the hydroxylation of tyrosine to dopa and subsequently to melanin generates significant quantities of reactive oxygen species. Making pigment is what damages the cell that makes it. The defense fails with AGE and the failure is measured: prematurely gray hair follicles demonstrate a decrease in catalase expression and activity, and a marked reduction in catalase results in millimolar accumulation of hydrogen peroxide. Millimolar, inside the shaft. And the damage is targeted at the pigment machinery itself: tyrosinase’s methionine residue 374 is particularly susceptible to H2O2-mediated oxidation, and the methionine SULFOXIDE reductase enzymes that repair oxidized methionine in tyrosinase and tyrosinase-related proteins are themselves inactivated. The peroxide bleaches the melanin and disables the enzyme that would replace it. And it explains a cell-type difference: compared with keratinocytes, melanocytes ARE more vulnerable to oxidative stress — and amelanotic melanocytes at the outer root sheath, which are not making pigment, survive longer even in white follicles. The ones doing the work are the ones that die. doi 10.1016/j.jid.2023.06.024 · PMID 24033376
It reduces Heart muscle cell.
The oxidative burden, and it moves with the dose. In the eam model, treatment 'induced a significant decrease of PROOXIDANTS production (O2⁻, H2O2, and TBARS) and improved antioxidant defense system via increase in GSH, SOD, and CAT... with medium and high dose being more effective than low dose' (pmc8901324 — Melissa officinalis l. Supplementation Provides Cardioprotection in a Rat Model of Experimental Autoimmune Myocarditis). ⇒ a redox shift alongside a recovery of pump function.
Blends that modulate it
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See it on the map
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