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DNA, oxidation

A method has been reported for the quantification of the DNA oxidation products, 8-hydroxy-2 -deoxyguanosine (8-OH-dG), 8-hydroxy-2 -deoxyadenosine (8-OH-dA), 5-hydroxymethyl-2-deoxyuridine (HMDU), thymidine glycol (TG) and 2-hydroxy-2 -deoxyadenosine (2-OH-dA) [37], The HPLC system employed consisted of a 2.0 X 250 mm Cig column and gradient elution from waterimethanol, (94 6) to (10 90) over 28 min, at a flow rate of 200 tilmin ... [Pg.279]

HARPER, A, KERR, D J, GESCHER, A and CHIPMAN K J (1999) Antioxidant effects of isoflavonoids and lignans, and protection against DNA oxidation. Free Rad Res. 31149-60. [Pg.82]

Frenkel, K., Zhong, Z., Wei, H., Karkoszka, J., Patel, U., Rashid, K., Georgescu, M. and Solomon, J.J. (1991). Quantitative high-performance liquid chromatography analysis of DNA oxidized in vitro and in vivo. Anal. Biochem. 196, 126-136. [Pg.212]

Fig. 9 Long-range oxidative damage in DNA is regulated by the structure of the DNA n-stack. Photoexcited [Rh(phi)2(bpy )]3+ intercalated within B-DNA oxidizes guanine doublets positioned 17 A and 40 A away with approximately equal efficiency. When a bulge is introduced in the DNA oxidation at the distal guanine doublet is inhibited. As shown by the NMR structure, bulges introduce local distortions in the DNA r-stack, although the kinking of the helical actually positions the distal guanine closer to the Rh(III) photooxidant... Fig. 9 Long-range oxidative damage in DNA is regulated by the structure of the DNA n-stack. Photoexcited [Rh(phi)2(bpy )]3+ intercalated within B-DNA oxidizes guanine doublets positioned 17 A and 40 A away with approximately equal efficiency. When a bulge is introduced in the DNA oxidation at the distal guanine doublet is inhibited. As shown by the NMR structure, bulges introduce local distortions in the DNA r-stack, although the kinking of the helical actually positions the distal guanine closer to the Rh(III) photooxidant...
Palozza, P. Serini, S. Di Nicuolo, R et al. 2004a. Beta-carotene exacerbates DNA oxidative damage and modifies p53-related pathways of cell proliferation and apoptosis in cultured cells exposed to tobacco smoke condensate. Carcinogenesis 25 1315-1325. [Pg.482]

The most commonly measured product of DNA oxidation is 8-hydroxy-deoxyguanosine (8-OHdG). This product is usually measured by HPLC methods however, the recent development of commercial ELISA kits is expanding research in this area. [Pg.279]

Xanthine oxidase, a widely used source of superoxide, has been frequently applied for the study of the effects of superoxide on DNA oxidation. Rozenberg-Arska et al. [30] have shown that xanthine oxidase plus excess iron induced chromosomal and plasmid DNA injury, which was supposedly mediated by hydroxyl radicals. Ito et al. [31] compared the inactivation of Bacillus subtilis transforming DNA by potassium superoxide and the xanthine xanthine oxidase system. It was found that xanthine oxidase but not K02 was a source of free radical mediated DNA inactivation apparently due to the conversion of superoxide to hydroxyl radicals in the presence of iron ions. Deno and Fridovich [32] also supposed that the single strand scission formation after exposure of DNA plasmid to xanthine oxidase was mediated by hydroxyl radical formation. Oxygen radicals produced by xanthine oxidase induced DNA strand breakage in promotable and nonpromotable JB6 mouse epidermal cells [33]. [Pg.837]

Furthermore, it was found that stimulated human neutrophils are able to produce 5-chloro-2 -deoxycytidine and that the myeloperoxidase system generates just the same levels of 5-chlorocytosine in DNA and RNA in vitro (Reaction (4), Figure 28.3). It is possible that myeloperoxidase-generated chlorinated products may modify nuclear acids of pathogens and nuclear acids in host cells during inflammation. Hawkins et al. [48] suggested that DNA oxidation may be initiated by protein chloramines formed in the reaction of HOCl with histones in the nucleosome. [Pg.838]

Lynn et al. [71] demonstrated the damaging effect of arsenite on DNA. It has been shown that arsenite at low concentrations increased DNA oxidative damage in vascular smooth muscle cells (VSMCs) that can be a cause of arsenite-induced atherosclerosis. Bruskov et al. [72] found that heat induced the formation of 8-oxoguanine in DNA solution at pH 6.8, which was supposedly mediated by oxygen radicals. [Pg.840]

Numerous studies were dedicated to the effects of flavonoids on microsomal and mitochondrial lipid peroxidation. Kaempferol, quercetin, 7,8-dihydroxyflavone and D-catechin inhibited lipid peroxidation of light mitochondrial fraction from the rat liver initiated by the xanthine oxidase system [126]. Catechin, rutin, and naringin inhibited microsomal lipid peroxidation, xanthine oxidase activity, and DNA cleavage [127]. Myricetin inhibited ferric nitrilotriacetate-induced DNA oxidation and lipid peroxidation in primary rat hepatocyte cultures and activated DNA repair process [128]. [Pg.863]

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],... [Pg.938]

Table 5.19 Analytical data obtained for the LC-MS determination of DNA oxidation products... Table 5.19 Analytical data obtained for the LC-MS determination of DNA oxidation products...

See other pages where DNA, oxidation is mentioned: [Pg.8]    [Pg.279]    [Pg.281]    [Pg.131]    [Pg.360]    [Pg.287]    [Pg.296]    [Pg.301]    [Pg.397]    [Pg.471]    [Pg.654]    [Pg.16]    [Pg.833]    [Pg.833]    [Pg.836]    [Pg.836]    [Pg.837]    [Pg.840]    [Pg.840]    [Pg.841]    [Pg.841]    [Pg.842]    [Pg.842]    [Pg.843]    [Pg.843]    [Pg.843]    [Pg.944]    [Pg.567]    [Pg.222]    [Pg.309]    [Pg.288]   
See also in sourсe #XX -- [ Pg.23 ]




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