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Lipid carcinogenesis

ZHANG L-x, CONNEY R V and BERTRAM J s (1991) Carotenoids enhance gap jrmctional communication and inhibit lipid peroxidation in C3H/1077/2 cells relationship to their cancer chemopreventative action . Carcinogenesis, 12, 2109-14. [Pg.279]

Palozza, P. et al., Dual role of beta-carotene in combination with cigarette smoke aqueous extract on the formation of mutagenic lipid peroxidation products in lung membranes dependence on pOj, Carcinogenesis, 2006. [Pg.190]

Yoshiji, H., Nakae, D., Mizumoto, Y., Horiguchi, K., Tamura, K., Denda, A., Tsujii, T. and Konishi, Y. (1992). Inhibitory effect of dietary iron deficiency on inductions of putative preneoplastic lesions as well as 8-hydroxydeoxyguanosine in DNA and lipid peroxidation in the livers of rats caused by exposure to a choline-deficient L-amino acid defined diet. Carcinogenesis 13, 1227-1233. [Pg.174]

Zhang, L. X., R. V. Cooney, and J. S. Bertram. 1991. Carotenoids enhance gap junctional communication and inhibit lipid peroxidation in C3H/10T1/2 cells Relationship to their cancer chemopreventive action. Carcinogenesis 12(11) 2109—2114. [Pg.434]

Sera N, Tokiwa H, Miyata N (1996) Mutagenicity of the fullerene C60-generated singlet oxygen dependent formation of lipid peroxides. Carcinogenesis 17 2163-2169. [Pg.105]

Fischer. The effect of dietary lipid on skin tumor promotion by benzoyl peroxide comparison of fish, coconut and comoil. Carcinogenesis 1991 12(6) 1023-1028. [Pg.144]

CN210 Berton, T. R., S. M. Fischer, C. J. Conti, and M. F. Locniskar. Comparison of ultraviolet light-induced skin carcinogenesis and ornithine decarboxylase activity in sencar and hairless SKH-1 mice fed a constant level of dietary lipid varying in com and coco-... [Pg.153]

The relationship between diet and cancer risk is extremely complex (7). Factors that appear to enhance carcinogenesis under one set of conditions may have no effect or even inhibit carcinogenesis under different conditions (2). The link between dietary fat and cancer is complicated by many factors, in particular total calorie intake and fatty acid composition (2). Among the fatty acids that comprise lipid, only linoleic acid is clearly linked to the enhancement of carcinogenesis in rat manunary gland (5), pancreas (4) and colon (5). [Pg.262]

Elliott, B.M. Elcombe, C.R. (1987) Lack of DNA damage or lipid peroxidation measured in vivo in the rat liver following treatment with peroxisomal proliferators. Carcinogenesis, 8, 1213-1218... [Pg.130]

Wang, M.Y. Liehr, J.G (1995) Lipid hydroperoxide-induced endogenous DNA adducts in hamsters possible mechanism of lipid hydroperoxide-mediated carcinogenesis. Arch. Biochem. Biophys., 316, 38-46... [Pg.432]

Chlorogenic and caffeic acids may play a role in the body s defense against carcinogenesis and mutagenesis by their antioxidant properties. The antioxidant and antiradical influences of chlorogenic acids on lipid peroxidation are not yet clear. Research has indicated that chlorogenic acids are an antioxidant, however, their complex antioxidant properties require systematic investigation in diverse directions. [Pg.940]

Fat-soluble vitamins, in addition to their antioxidative effects on lipids, appear to exert a general protective effect in animals. Vitamin A and beta-carotenes protect lab animals from toxicity of citral, cyclophosphamide and some hydrocarbons (Seifter et al, (A2.) In related but independent studies, it was observed that high levels of vitamin A inhibit tumorogenesis and that low levels of vitamin A appear to enhance tumorogenesis (Baird, (1 ). vitamin E inhibited chemically-induced carcinogenesis in test systems (Shamberger, ) and also reduced the susceptibility of rats to cigarette smoke (Chow,... [Pg.16]

In summary, it is clear that a multitude of dietary factors can Influence the metabolism of xenobiotics, particularly those that can be involved in carcinogenesis. We are and will continue to be exposed to xenobiotics of various types from our food, industrial sources, toxic wastes, drugs, and smoke. The well nourished animal or man appears, within the limits of individual variation, to be able to metabolize and excrete most of these xenobiotics harmlessly. It is important that we use the best diet possible to reduce fat in the diet, particularly where lipid... [Pg.16]

Fats and Lipids. Of all the dietary components studied, the combined epidemiological and experimental evidence is most suggestive for a causal relationship between high fat intake and increased occurrence of cancer. The relationship between dietary cholesterol and carcinogenesis is not clearly understood. [Pg.22]

In addition to cytochrome P-450 induction, other diet induced metabolic effects are likely to be involved in carcinogenesis. High temperature processing or long-term storage of foods with attendant exposure to oxygen can lead to the formation of lipid peroxides and oxidized sulfur amino acids in the food. The partially oxidized S-amino acids cystine monoxide (CMO) and methionine sulfoxide (MSO) are nutritionally available, but require in vivo conversion to the reduced amino acids at the... [Pg.156]

The mechanism whereby dietary protein influences DMH carcinogenesis is unknown. An attractive hypothesis concerning the effects of dietary protein on DMH metabolism is discussed later in this manuscript. Another factor which may contribute to tumor growth promotion in the intestine is a doubling of fecal crude lipid excretion which we observed in mice as dietary protein was increased from 10 to 40% of the diet (19). The association between... [Pg.294]


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See also in sourсe #XX -- [ Pg.142 ]




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Carcinogenesis

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