Oxidative damage, inflammation

A series of natural and synthetic products have also shown antiamyloid properties as amyloid scavengers or P-breakers. One example is the phenolic yellow curry pigment curcumin, which has potent anti-inflammatory and antioxidant activities and can suppress oxidative damage, inflammation, cognitive deficits, and amyloid... 

The risk of developing colonic cancer is raised in UC, particularly in those with long-standing extensive disease (Lennard-Jones et al., 1990). The mechanism of this increased susceptibility is unknown, although it is tempting to speculate that it is related to inflammation and resulting oxidative damage to DNA. As yet there is little evidence to support this contention. Markowitz et al. (1988) have reported a decrease in constituent and oxidant-induced adenosine diphosphate ribosyl... 

A number of early in vitro studies demonstrated a considerable role of free radicals in liver injury (see, for example, Proceedings of International Meeting on Free Radicals in Liver Injury [341]). Later on, it was shown that chronic inflammation in the liver-induced oxidative DNA damage stimulated chronic active hepatitis and increased the risk of hepatocarcinogenesis [342,343]. Farinati et al. [344] showed that 8-OHdG content increased in circulating leukocytes of patients with chronic hepatitis C virus (HCV) infection. DNA oxidative damage is supposedly an early event of HCV-related hepatitis. The formation of isoprostanes in the liver of carbon tetrachloride-treated rats can be suppressed by the administration of vitamin E [345],... 

The inflammatory response changes with time and can be divided into phases. The rapid phase occurs within seconds to minutes and consists of vasodilation, increased blood flow, edema, and pain. The acute phase is characterized by induction of inflammatory genes by NF-kB and other transcription factors. During this phase, moderate amounts of inflammatory mediators are produced. The chronic phase occurs over months to years and is marked by dramatically increased production of inflammatory mediators. The secondary chronic phase of inflammation occurs after years of oxidative damage has degraded blood vessels and tissues. Such chronic inflammation appears to play a role in many disease states, such as arteriosclerosis and cancer. 

What are the possible adverse consequences of accumulation of the A(3 protein It may cause inflammation by activation of microglia,1157 which may cause damage by release of NO.1206 A(3 may induce death of neurons by apoptosis.1201 1207-1209 A defect in protesomal degradation may be a factor.1208 Both Ap and the prion protein may promote oxidative damage. The brain derives most of its energy from oxidative metabolism, a major source of damaging radicals. Mitochondria are found in dendrites as well as cell bodies.1210 Methionine residues in glycine-rich parts of the AP and prion proteins are suspected as centers of free radical formation.1202 1211... 

Martin AR, Villegas I, La Casa C, de la Lastra CA. 2004. Resveratrol, a polyphenol found in grapes, suppresses oxidative damage and stimulates apoptosis during early colonic inflammation in rats. Biochem Pharmacol 67 1399-1410. 

Beal ME Mitochondria, oxidative damage, and inflammation in Parkinson s disease. Arm N YAcad Sci. 2003 991 120-131. 

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. 

K8. Kaur, H., and Halliwell, B., Evidence for nitric oxide-mediated oxidative damage in chronic inflammation Nitrotyrosine in serum and synovial fluid from rheumatoid patients. FEBS Lett. 350, 9-12(1994). 

In a series of studies, several molecular mechanisms for antifibrotic effects of pirfenidone have been established. As discussed earlier, BL induces oxidative damage in lungs by stimulating the generation of ROS (20), which are responsible for various stages of the inflammation and lipid peroxidation followed by fibrosis. 

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