Cartilage glutathioneHuman cells2023
Nrf2, the master switch for a cell's antioxidant defences, was about 40% lower in cartilage cells from older adults and about 50% lower in osteoarthritic cells than in younger cells. Oxidative stress raised it nearly fourfold in young cells but not in old ones.
Age and oxidative stress regulate Nrf2 homeostasis in human articular chondrocytes.
Cartilage glutathioneHuman tissueAnimal2022
GPX4, the glutathione-dependent enzyme that stops ferroptosis, was lower in damaged cartilage from 55 osteoarthritis patients than in undamaged cartilage. Lowering it made cartilage cells more sensitive to oxidative stress and worsened osteoarthritis in an animal model.
Contribution of ferroptosis and GPX4's dual functions to osteoarthritis progression.
Cartilage glutathioneReviewAnimal2020
Glutathione was more plentiful in cartilage than in the meniscus or the knee's fat pad, but more prone to age-related oxidation. Under compressive loading it oxidised and needed unloaded periods to recover.
Glutathione as a mediator of cartilage oxidative stress resistance and resilience during aging and osteoarthritis.
Cartilage glutathioneReview2019
A review of the evidence that, with age, cartilage cells make more reactive oxygen species than their antioxidant defences can handle, which disrupts their signalling and contributes to cartilage breakdown and cell death.
Reactive oxygen species, aging and articular cartilage homeostasis.
Cartilage glutathioneHuman cells2019
In cartilage cells from healthy human cartilage, hydrogen peroxide, an inflammatory signal and calcium crystals each lowered SOX9 and raised the cartilage-cutting enzymes MMP13 and ADAMTS5.
Altered expression of the core circadian clock component PERIOD2 contributes to osteoarthritis-like changes in chondrocyte activity.
Cartilage glutathioneHuman cellsAnimal2016
Cartilage cells from older adults showed more oxidative damage to their peroxiredoxin antioxidants, which switched off a survival signal and switched on a death signal. Mice protected from mitochondrial oxidants developed less age-related osteoarthritis.
Oxidative Stress Promotes Peroxiredoxin Hyperoxidation and Attenuates Pro-survival Signaling in Aging Chondrocytes.
Cartilage glutathioneReview2009
A review of articular cartilage: it has no blood vessels, lymphatics or nerves, and its cells, the chondrocytes, make up only about 2% of its volume.
The basic science of articular cartilage: structure, composition, and function.
Cartilage glutathioneHuman cells2003
More than twice as many cartilage cells from donors aged 50 and over died under oxidant stress as cells from donors aged 18 to 49. The older cells held more of their glutathione in its used form, and cells drained of glutathione died more readily.
Increased oxidative stress with aging reduces chondrocyte survival: correlation with intracellular glutathione levels.
How glutathione is madeReview2013
A review of glutathione synthesis. The two key controls are the supply of cysteine and the activity of the first enzyme in the pathway, glutamate cysteine ligase.
Glutathione synthesis.
How glutathione is madeReview2009
An overview of glutathione, the most abundant small thiol that cells make, and its roles in protecting cells from oxidative damage and keeping their redox balance.
Glutathione: overview of its protective roles, measurement, and biosynthesis.
Precursors in peopleHuman trial2023
In a 16-week placebo-controlled trial in 24 older adults, GlyNAC corrected glutathione deficiency and improved oxidative stress, inflammation, gait speed and muscle strength. Placebo did not.
Supplementing Glycine and N-Acetylcysteine (GlyNAC) in Older Adults Improves Glutathione Deficiency, Oxidative Stress, Mitochondrial Dysfunction, Inflammation, Physical Function, and Aging Hallmarks: A Randomized Clinical Trial.
Precursors in peopleHuman trial2022
In 114 healthy older adults over two weeks, GlyNAC at 2.4 to 7.2 g a day did not raise glutathione across the whole group. It did raise it in those with high oxidative stress and low starting glutathione.
A Randomized Controlled Clinical Trial in Healthy Older Adults to Determine Efficacy of Glycine and N-Acetylcysteine Supplementation on Glutathione Redox Status and Oxidative Damage.
Precursors in peopleHuman study2021
In an open-label pilot, 24 weeks of glycine plus N-acetylcysteine (GlyNAC) corrected red-cell glutathione deficiency and oxidative stress in older adults and improved strength and gait speed. The gains declined within 12 weeks of stopping.
Glycine and N-acetylcysteine (GlyNAC) supplementation in older adults improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial dysfunction, genotoxicity, muscle strength, and cognition: Results of a pilot clinical trial.
Precursors in peopleHuman study2011
Eight older adults had lower red-cell glycine, cysteine and glutathione and made glutathione more slowly than younger adults. Two weeks of cysteine and glycine raised their glutathione by about 95% and lowered markers of oxidative stress.
Deficient synthesis of glutathione underlies oxidative stress in aging and can be corrected by dietary cysteine and glycine supplementation.
Oral glutathioneHuman study2018
In a one-month pilot in 12 healthy adults, liposomal glutathione at 500 or 1,000 mg a day raised blood glutathione and lowered markers of oxidative stress.
Oral supplementation with liposomal glutathione elevates body stores of glutathione and markers of immune function.
Oral glutathioneHuman trial2015
Over six months, 250 or 1,000 mg a day of oral glutathione raised glutathione in blood cells, plasma and cheek cells of 54 healthy adults, by 30 to 35% in red cells, plasma and lymphocytes at the higher dose.
Randomized controlled trial of oral glutathione supplementation on body stores of glutathione.
Oral glutathioneHuman study1992
A single 3 g dose of oral glutathione did not raise plasma glutathione in seven healthy volunteers. The authors put this down to glutathione being broken down in the gut and liver.
The systemic availability of oral glutathione.
N-acetylcysteineLabAnimal2026
NAC delivered to cartilage cells in targeted nanoparticles restored their glutathione under mechanical stress and, injected into mouse knees, reduced cartilage breakdown. The effect needed GPX4.
Chondrocyte-Targeted Nanoparticles Loaded with N-Acetylcysteine Protect Articular Cartilage and Attenuate Osteoarthritis by Inhibiting Ferroptosis via Glutathione Maintenance.
N-acetylcysteineLabAnimal2019
NAC given by mouth held back MMP13, the loss of type II collagen and cartilage cell death, and significantly slowed osteoarthritis development in rats.
Oral administration of N-acetyl cysteine prevents osteoarthritis development and progression in a rat model.
N-acetylcysteineLabAnimal2010
NAC protected cartilage cells from nitric oxide-induced death, and the protection vanished when glutathione synthesis was blocked. Injected into rat knees, NAC reduced cartilage damage.
N-acetylcysteine prevents nitric oxide-induced chondrocyte apoptosis and cartilage degeneration in an experimental model of osteoarthritis.
GlycineLab2018
Raising glycine above 1 mM increased type II collagen production by cartilage cells by 60 to 75%, a larger and longer-lasting effect than proline or lysine.
High glycine concentration increases collagen synthesis by articular chondrocytes in vitro: acute glycine deficiency could be an important cause of osteoarthritis.
GlycineReview2009
An analysis of human glycine supply. The body makes about 3 g a day and food adds 1.5 to 3 g, which may fall about 10 g a day short of all its uses, collagen included.
A weak link in metabolism: the metabolic capacity for glycine biosynthesis does not satisfy the need for collagen synthesis.
GlutamineAnimalLab2020
Cartilage cells' identity was tied to glutamine use. SOX9 raised glutamine uptake, and glutathione made from glutamine kept reactive oxygen species down so the cells could survive without a blood supply.
Glutamine Metabolism Controls Chondrocyte Identity and Function.
GlutamineLab2006
Glutamine almost completely prevented the loss of cartilage cells under heat stress and nitric oxide, alongside a rise in the protective protein HSP70.
Glutamine protects articular chondrocytes from heat stress and NO-induced apoptosis with HSP70 expression.
Alpha-lipoic acidLabAnimal2026
Dihydrolipoic acid, the active form of lipoic acid, protected cartilage cells' glutathione and GPX4, suppressed ferroptosis and slowed cartilage damage in mice.
Dihydrolipoic acid suppresses ferroptosis in chondrocytes to ameliorate the progression of osteoarthritis by modulating the FOXO1/TXNIP signaling pathway.
Alpha-lipoic acidAnimal2016
In rats, alpha-lipoic acid lessened cartilage damage, raised collagen type II and aggrecan gene activity and lowered markers of oxidative damage.
Chondroprotective effects of alpha-lipoic acid in a rat model of osteoarthritis.
Alpha-lipoic acidLab1997
Lipoic acid, once reduced, raised cells' own glutathione by helping them take up cysteine. It mainly restored cells that were short of glutathione rather than pushing healthy cells higher.
Lipoic acid increases de novo synthesis of cellular glutathione by improving cystine utilization.
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