Reactive oxygen species
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Reactive oxygen species (ROS) include oxygen ions, free radicals and peroxides both inorganic and organic. They are generally very small molecules and are highly reactive due to the presence of unpaired valence shell electrons. ROSs form as a natural byproduct of the normal metabolism of oxygen but can damage cell membranes by causing oxidative stress. Cells are normally able to defend themselves against ROS damage through the use of the enzymes superoxide dismutase (SOD) and catalase .
The effects of ROS on cell metabolism have been well documented in a variety of species. These include not only roles in programmed cell death and apoptosis, but also positive effects such as the induction of host defense genes and mobilisation of ion transport systems. This is implicating them more frequently with roles in oxidative signalling. In particular, platelets involved in wound repair and blood homeostasis release ROS to recruit additional platelets to sites of injury. These also provide a link to the adaptive immune system via the recruitment of leukocytes
Reactive oxygen species are implicated in cellular activity to a variety of inflammatory responses including cardiovascular disease and hearing impairment via cochlear damage induced by elevated sound levels.
References
- Sen, C.K. (2003) The general case for redox control of wound repair, Wound Repair and Regeneration, 11, 431-438
- Krötz, F., Sohn, HY., Gloe, T., Zahler, S., Riexinger, T., Schiele, T.M., Becker, B.F., Theisen, K., Klauss, V., Pohl, U. (2002) NAD(P)H oxidase-dependent platelet superoxide anion release increases platelet recruitment, Blood, 100, 917-924
- Pignatelli, P. Pulcinelli, F.M., Lenti, L., Gazzaniga, P.P., Violi, F. (1998) Hydrogen Peroxide Is Involved in Collagen-Induced Platelet Activation, Blood, 91 (2), 484-490
- Guzik, T.J., Korbut, R., Adamek-Guzik, T. (2003) Nitric oxide and superoxide in inflammation and immune regulation, Journal of Physiology and Pharmacology, 54 (4), 469-487