Peroxides proteins

Several studies have demonstrated that treatment of diabetic patients with the sulphonylurea, gliclazide, is associated with a fall in lipid peroxidation, protein fluorescence and beneficial effects on platelet function (Florkowski et al., 1988 Jennings et al., 1992). These changes were seen to be independent of changes in giycaemic control. 

Peroxidases oxidize tyrosines, both as a free amino acid and as a residue in peptides and proteins. When proteins are treated with HRP in the presence of hydrogen peroxide, protein dimers are obtained through the coupling of tyrosyl radicals. HRP can also be used for cross-linking of proteins with polysaccharides [35]. In this case, coupling occurs between a tyrosyl radical in the protein and a radical species on the saccharide ... 

Nitrite is also an important source of nitric oxide, molecule that could rapidly react with superoxide to form peroxynitrite (ONOO ), a potent cytokine which is very reactive (Kohn et al., 2002). Reactive species of oxygen and nitrogen could initiate a toxic oxidative chain, including lipid peroxidation, protein oxidation, directly inhibiting some enzymes from the mitochondrial respiratory chain, and causing dysfunctions of the antioxidant defense systems. 

Jain SK and Lim G (2001) Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation, and (Na+ + K+)-ATPase activity reduction in high glucose-treated human erythrocytes. Free Radicals in Biology and Medicine 30,232-7. 

Keywords DNA oxidation Lipid peroxidation Protein oxidation Adduct ... 

Keywords Aldehydes isoketals levuglandins lipid peroxidation protein modification... 

Fig 24.23. A model for the role of ROS and RNOS in neuronal degradation in Parkinson s disease. 1. Dopamine levels are reduced by monoamine oxidase, which generates H2O2. 2. Superoxide also can be produced by mitochondria, which SOD will convert to H2O2. Iron levels increase, which allows the Fenton reaction to proceed, generating hydroxyl radicals. 3. NO, produced by inducible nitric oxide synthase, reacts with superoxide to form RNOS. 4. The RNOS and hydroxyl radical lead to radical chain reactions that result in Upid peroxidation, protein oxidation, the formation of lipofuscin, and neuronal degeneration. The end result is a reduced production and release of dopamine, which leads to the clinical symptoms observed. 

The first process, H-abstraction, may initiate an important generic reaction of amino acids (Fig. 4). Radicals attributed to the a-carbon have been identified by electron spin resonance (ESR) of peroxidized proteins (22). Further reaction with O2 (hypothetical) would lead to amino acid hydroperoxides. A different pathway to amino acid hydroperoxide has been proposed by Yong and Karel (23), but their proposal involves an indirect pathway to the a-carbon radical. Homolysis of the hydroperoxy group would afford an amino acid oxy radical susceptible to p-scission via Reaction G. Thus, p-scission between the a-carbon and the amino group may explain the increase in amide content of protein that has been peroxidized in dry systems, as well as the coincident protein chain scission observed... 

Kirkland JB. Lipid peroxidation, protein thiol oxidation and DNA damage in hydrogen peroxide-induced injury to endothelial cells Role of activation of poly(ADP-ribose)polymetasc. Biochim Biophys Acta 1991 1092 319-25. 

Hu, J., Speisky, H., Cotgreave, I. A. (1995). The inhibitory effects of boldine, glaucine, and probucol on TPA -induced down regulation of gap junction function relationships to intracellular peroxides, protein kinase C translocation, and cotmexin 43 phosphorylation. Biochem. Pharmacol, 50(10), 1635-1643. 

Vitamin Bg in its various forms has antioxidant properties that compare favorably with those of the well-established antioxidant vitamins such as vitamin C and the tocopherols. Pyridoxine and pyridoxamine inhibit superoxide radicals and prevent lipid peroxidation, protein glycosylation, and Na+,K+-ATPase activity in high glucose-treated erythrocytes and hydrogen peroxide-treated monocytes (2) and endothelial cells (3). In bovine endothelial cells, treatment with homocysteine and copper increased extracellular hydrogen peroxide levels. Treatment with pyridoxal or EDTA prevented such increases and enhanced the viability of the cells by supporting apoptosis. 

These chemical criteria have been subsequently substantiated in abundance in vitro experiments involving the antioxidant action of polyphenols against lipid peroxidation, protein oxidation, and DNA damage, as well as in models of neurodegeneration (Youdim et al, 2004 Frade et al, 2005). 

The rate constants for the free-radical-induced haemolysis of human erythrocytes have been calculated from haemolysis curves and compared with those obtained from experiments with erythrocyte ghosts treated with various radical initiators. The authors concluded that their reaction model (lipid peroxidation/protein oxidation) may be useful in analysing radical-induced haemolysis. In recent years there has been considerable interest in the role the 1-hydroxyethyl radical in the toxic effects of ethanol. Recent studies have shown that the 1-hydroxyethyl radical inactivates the antioxidant enzymes glutathione reductase, glutathione oxidase, and superoxide dismutase. These results indicate that a prolonged generation of the 1-hydroxyethyl radical in animal cells may lower the antioxidant defence status, thus contributing to oxidative stress and toxicity. ... 

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