Oxidative damage to tissues

Feng, Y-H. Hart, G. In vitro Oxidative Damage to Tissue-Type Plasminogen Activator a Selective Modification of the Biological Functions. Cardiovasc. Res., 1995,30, 255. 

SP 131 describes Pauling s 1933 discovery and verification of the superoxide free radical, which now, 67 years later—has become of much interest as an active agent in oxidative damage to tissues and in the aging process. The control of this substance in living organisms, by means of the superoxide dismutase enzyme that catalyzes its decomposition, is an example of a potential task of orthomolecular medicine (see below). 

Sadrzadeh, S.M.H. and Eaton, J.W. (1992). Hemt obin-induced oxidant damage to the central nervous system. In Free Radical Mechanisms of Tissue Injury (eds. M.T. Moslen and C.V. Smith) pp. 24—32. CRC Press, Boca Baton. 

Allopurinol also inhibits reperfusion injury. This injury occurs when organs that either have been transplanted or have had their usual blood perfusion blocked are reperfused with blood or an appropriate buffer solution. The cause of this injury is local formation of free radicals, such as the superoxide anion, the hydroxyl free radical, or peroxynitrite. These substances are strong oxidants and are quite damaging to tissues. 

The evidence for a pathophysiological role of oxidants in connective tissue injury is not confined to oxidative damage to the component macromolecules. Since there is reasonable indirect evidence that ROIs are released into the articular joint space during inflammation, it is likely that ROIs released from inflammatory cells which are adherent to or in contact with the articular cartilage surface might also damage the cellular components of articular cartilage. 

P7. Park, E. M., Park, Y. M., and Gwak, Y. S., Oxidative damage in tissues of rats exposed to cigarette smoke. Free Radicals Biol. Med. 25, 79-86 (1998). 

On the other hand, oxidative stress has also been found to induce PSl transcription, thereby promoting production of pathological levels of Af) in AD (Tamagno et al., 2008). Indeed, it has been proposed that the pathophysiology of oxidative stress is reflected in damage to tissue biomolecules, including lipids, proteins, and DNA by free radicals (Migliore and Coppede, 2009). 

Similar studies of lipid peroxidation products have been performed for other substrate lipids. Of particular interest are oxidation produets of docosahexaenoic acid (DHA), which have been termed F4-neuroprostanes (F4-NeuroPs) (Roberts et al, 1998). In contrast to AA, which is evenly distributed in all eell types in all tissues, DHA is highly eoneentrated in neuronal membranes (Salem et al, 1986 Montine et al, 2004). Thus, determination of F4-NeuroPs permits the speeifle quantifleation of oxidative damage to neuronal membranes in vivo (Montine et al, 2004). In faet, to our knowledge, F4-NeuroPs are the only quantitative in vivo marker of oxidative damage that is selective for neurons. 

---