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 and have important roles in cell signaling. However, during times of environmental stress ROS levels can increase dramatically, which can result in significant damage to cell structures. This cumulates into a situation known as oxidative stress. Cells are normally able to defend themselves against ROS damage through the use of enzymes such as superoxide dismutases and catalases. Small molecule antioxidants such as ascorbic acid (vitamin-C), uric acid, and glutathione also play important roles as cellular antioxidants. Similarly, polyphenol antioxidants assist in preventing ROS damage by scavenging free radicals. In contrast, the antioxidant ability of the extracellular space in relatively less--e.g., the most important plasma antioxidant in humans is probably uric acid.
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 defence genes and mobilisation of ion transport systems. This is implicating them more frequently with roles in redox signaling or oxidative signaling. 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. They may also be involved in hearing impairment via cochlear damage induced by elevated sound levels, ototoxicity of drugs such as cis-platin, and in congenital deafness in both animals and humans. Redox signaling is also implicated in mediation of apoptosis or programmed cell death and ischaemic injury. Specific examples include stroke and heart attack.
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- 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
- Free Radicals and Human Disease, a Review
