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Free radicals defence mechanisms

The free-radical defence mechanisms utilized by the brain are similar to those found in other tissues. The enzymes SOD, catalase, glutathione peroxidase, and the typical radical scavengers, ascorbate, vitamin E and vitamin A are present in the brain, as they are in peripheral tissues. However, the brain may actually be slightly deficient in some of these defence mechanisms when compared to the amounts present in other tissues. [Pg.77]

Diabetic patients have reduced antioxidant defences and suffer from an increased risk of free radical-mediated diseases such as coronary heart disease. EC has a pronounced insulin-like effect on erythrocyte membrane-bound acetylcholinesterase in type II diabetic patients (Rizvi and Zaid, 2001). Tea polyphenols were shown to possess anti-diabetic activity and to be effective both in the prevention and treatment of diabetes (Choi et al, 1998 Yang et al, 1999). The main mechanism by which tea polyphenols appear to lower serum glucose levels is via the inhibition of the activity of the starch digesting enzyme, amylase. Tea inhibits both salivary and intestinal amylase, so that starch is broken down more slowly and the rise in serum glucose is thus reduced. In addition, tea may affect the intestinal absorption of glucose. [Pg.138]

This chapter addresses (1) the mechanisms, antioxidant defences and consequences in relation to free-radical production in the inflamed rheumatoid joint (2) lipid abnormalities in RA (3) the potential contribution of ox-LDL to RA (the role of ox-LDL in coronary heart disease is discussed in Chapters 2 and 3 and will not be fully discussed here) and (4) the therapeutic aspects of chain-breaking antioxidant interventions in RA. [Pg.98]

Mechanisms, Antioxidant Defences and Consequences of Free-radical Production in the Rheumatoid Joint... [Pg.98]

The efficient removal of O2 and H2O2 vvill diminish OH formation and therefore antioxidant defence systems have evolved to limit their accumulation. Enzymic and low molecular weight antioxidants exist to scavenge free radicals as self-protection mechanisms. Some proteins exhibit antioxidant properties because they chelate transition-metal catalysts. The significance of antioxidants in relation to inflammatory joint disease is discussed below. [Pg.100]

Wohaieb, S.A. and Godin, D.V. (1987). Alterations in free radical tissue-defence mechanisms in streptozocin-induced diabetes in rat. Diabetes. 36, 1014-1018. [Pg.198]

As an indirect effect of increased metal uptake, the physiological state of the cell can alter and defence mechanisms can be induced. Phytochelatin (metal binding proteins) synthesis and induction of free radical quenching enzymes and metabolites were frequently observed. Especially the latter can protect membranes against oxidative breakdown. [Pg.172]

Hager K, Marahrens A, Kenklies M, Riederer P, Munch G (2001) Alpha-Upoic add as a new treatment option for Azheimer type dementia. Arch Gerontol Geriatr 32 275-282 HalliweU B (1999) Antioxidant defence mechanisms from the beginning to the end (of the beginning). Free Radic Res 31 261-272... [Pg.623]

Antioxidant defences can be divided into five categories avoidance (sheltering), antioxidant enzymes (prevention), free-radical scavengers (containment), repair mechanisms (first aid) and stress responses (entrenchment). Some organisms, particularly those that hide from oxygen, rely on just one or two of these mechanisms, while others, including ourselves, draw on the entire armoury. We are, truly, antioxidant machines. To see... [Pg.195]

Oxidative stress is a condition in which free radicals and their products are present in excess of antioxidant defence mechanisms, leading to oxidative damage and structural and functional modifications of proteins, DNA, and RNA. Radicals can be formed through different mechanisms. ROS are formed by the reduction of molecular oxygen to water superoxide (O "), peroxyl radical (OH ), and hydrogen peroxide (H O ). RNS (NO and peroxynitrite) can also cause oxidative stress. [Pg.501]

The respiratory chain is the major source of oxygen free radicals. In theory, molecular oxygen should be completely reduced in complex IV by four electrons from water without the formation of intermediates. In practice, sometimes partial reduction occurs with oxygen being converted to superoxide anion radicals (Fig. 15.1). Also, the ubiquinone reactions in complexes I and II have an unfortunate tendency to leak electrons directly to oxygen. Overall, up to 2% of cellular oxygen forms superoxide free radicals and the body has developed defence mechanisms to counter their damaging effects. [Pg.39]

Defence mechanisms against free radicals and reactive oxygen species... [Pg.39]


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See also in sourсe #XX -- [ Pg.39 ]




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