Oxidation carcinogenesis

Both intestinal- and diffuse-type gastric adenocarcinomas are associated with 77. pylori infection. Since chronic inflammation has been associated with carcinogenesis, " the infection-inflammation pathway appears to be one of the major factors in carcinogenesis. Oxidative stress can be induced by infiltrating neutrophils and macrophages as well as the injected Cag proteins. This has been well summarized in a recent review."" Further studies are necessaiy to reveal the exact mechanism of 77. pj/oH-associated adenocarcinogenesis. 

Animal studies have shown that teas are effective in blocking or slowing carcinogenesis (121,131,133). Administration of teas or tea polyphenols to mice or rats have also been shown to decrease oxidative biomarkers, suggesting that tea polyphenols act as antioxidants (125,134). 

Cobalt compounds can be classified as relatively nontoxic (33). There have been few health problems associated with workplace exposure to cobalt. The primary workplace problems from cobalt exposure are fibrosis, also known as hard metal disease (34,35), asthma, and dermatitis (36). Finely powdered cobalt can cause siUcosis. There is Htfle evidence to suggest that cobalt is a carcinogen in animals and no epidemiological evidence of carcinogenesis in humans. The LD q (rat) for cobalt powder is 1500 mg/kg. The oral LD q (rat) for cobalt(II) acetate, chloride, nitrate, oxide, and sulfate are 194, 133, 198, 1700, 5000, and 279 mg/kg, respectively the intraperitoneal LD q (rat) for cobalt(III) oxide is 5000 mg/kg (37). 

Epoxides are often encountered in nature, both as intermediates in key biosynthetic pathways and as secondary metabolites. The selective epoxidation of squa-lene, resulting in 2,3-squalene oxide, for example, is the prelude to the remarkable olefin oligomerization cascade that creates the steroid nucleus [7]. Tetrahydrodiols, the ultimate products of metabolism of polycyclic aromatic hydrocarbons, bind to the nucleic acids of mammalian cells and are implicated in carcinogenesis [8], In organic synthesis, epoxides are invaluable building blocks for introduction of diverse functionality into the hydrocarbon backbone in a 1,2-fashion. It is therefore not surprising that chemistry of epoxides has received much attention [9]. 

WEI H, CAO Q AND RAHN R o (1996) Inhibition of UV light- and Fenton reaction-induced oxidative DNA damage by the soybean isoflavone genistein. Carcinogenesis. 17 (1) 73-7. 

Biochemical Properties and Physiological Roles of 3-Oxidized Ni-trosamines in Relation to their Carcinogenesis. 

The experiments with deuterium-labeled nitrosamines illustrate two important points. One is that oxidation of nitrosamines takes place at more than one position in the molecule, and the outcome of the balance of such competing reactions probably is the determinant of carcinogenic potency. The second is that the reason for the failure of carcinogenesis to be mirrored in many cases by the microsomally activated bacterial mutagenicity is that there can be several metabolic steps leading to formation of the proximate carcinogenic agent and not all of these need necessarily involve microsomal enzymes. ... 

Trush, M.A. and Kensler, T.W. (1991). An overview of the relationship between oxidative stress and chemical carcinogenesis. Free Rad. Biol. Med. 10, 210-219. 

Weitzman, S.A. and Gordon, L.l. (1990). Inflammation and cancer role of phagocyte-generated oxidants in carcinogenesis. Blood 76, 655-663. 

Claycamp, H.G. (1992). Phenol sensitization of DNA to subsequent oxidative damage in 8-hydroxyguanine assays. Carcinogenesis 13, 1289-1292. 

Kasprzak, K.S., Diwan, B.A., Rice, J.M., Misra, M., Riggs, C.W., Olinski, R and Dizdaroglu, M. (1992). Nickel(II)-mediated oxidative DNA base damage in renal and hepatic chromatin of pregnant rats and their fetuses. Possible relevance to carcinogenesis. Chem. Res. Tox. 5, 810-815. 

Loft, S., Vistisen, K., Ewertz, M., Tjonneland, A., Overvad, K. and Poulsen, H.E. (1992). Oxidative DNA damage estimated by 8-hydroxydeoxyguanosine excretion in humans influence of smoking, gender and body mass index. Carcinogenesis 13, 2441-2447. 

Oikawa, S. Hirosawa, I. Hirakawa, K. Kawanishi, S. Site specificity and mechanism of oxidative DNA damage induced by carcinogenic catechol. Carcinogenesis 2001, 22, 1239-1245. 

Bodell, W. J. Ye, Q. Pathak, D. N. Pongracz, K. Oxidation of eugenol to form DNA adducts and 8-hydroxy-2 -deoxyguanosine role of quinone methide derivative in DNA adduct formation. Carcinogenesis 1998, 19, 437 143. 

Potter, G. A. McCague, R. Jarman, M. A mechanistic hypothesis for DNA adduct formation hy tamoxifen following hepatic oxidative metaholism. Carcinogenesis 1994,5, 439 142. 

Alija, AJ, Bresgen, N, Sommerburg, O, Langhans, CD, Siems, W, and Eckl, PM, 2006. (1-Carotene breakdown products enhance genotoxic effects of oxidative stress in primary rat hepatocytes. Carcinogenesis 27, 1128-1133. 

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