Reactive oxygen species
Reactive oxygen species (ROS) are oxygen-containing molecules, such as superoxide and hydrogen peroxide, that react readily with fats, proteins and DNA. Cells make them as by-products of normal metabolism and use some of them as signals.
Also called ROS, oxidants.
The ROS made by chondrocytes that have drawn the most research attention are superoxide, hydrogen peroxide, nitric oxide (strictly a reactive nitrogen species) and peroxynitrite, which forms from nitric oxide (Bolduc 2019). Age-related decline in the mitochondria, the cell's power plants, and lower activity of the mitochondrial enzyme SOD2 are part of why chondrocyte ROS rise with age (Bolduc 2019).
In excess, ROS damage molecules and disrupt redox-regulated signalling (Bolduc 2019). In cells from healthy human cartilage, hydrogen peroxide lowered SOX9 and raised the cartilage-cutting enzymes MMP13 and ADAMTS5 (Rong 2019). Mice engineered to make catalase, a hydrogen peroxide-clearing enzyme, inside their mitochondria developed less age-related osteoarthritis (Collins 2016).
Glutathione is one of the cell's main ways of keeping them in check (Forman 2009). In rabbit cartilage cells in the lab, NAC prevented the surge in ROS triggered by nitric oxide, and its protection depended on glutathione (Nakagawa 2010).
Sources
- Bolduc JA, Collins JA, Loeser RF. Reactive oxygen species, aging and articular cartilage homeostasis. Free Radic Biol Med 2019.
- Rong J, Zhu M, Munro J et al. Altered expression of the core circadian clock component PERIOD2 contributes to osteoarthritis-like changes in chondrocyte activity. Chronobiol Int 2019.
- Collins JA, Wood ST, Nelson KJ et al. Oxidative Stress Promotes Peroxiredoxin Hyperoxidation and Attenuates Pro-survival Signaling in Aging Chondrocytes. J Biol Chem 2016.
- Forman HJ, Zhang H, Rinna A. Glutathione: overview of its protective roles, measurement, and biosynthesis. Mol Aspects Med 2009.
- Nakagawa S, Arai Y, Mazda O et al. N-acetylcysteine prevents nitric oxide-induced chondrocyte apoptosis and cartilage degeneration in an experimental model of osteoarthritis. J Orthop Res 2010.
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