Download Arachidonic Acid Metabolism and Tumor Initiation by Charles M. King (auth.), Lawrence J. Marnett (eds.) PDF

By Charles M. King (auth.), Lawrence J. Marnett (eds.)

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Cancer Res (38), 1479-1496, 1978. Miller EC, Miller JA, Hartman HA: N-hydroxy-2-acetylaminofluorene, a metabolite of 2-acetylaminofluorene with increased carcinogenic activity in the rat. Cancer Res (31): 815-824, 1961. ) (159): 1351-1353, 1968. Miller EC, Miller JA: The presence and significance of bound aminoazo dyes in the livers of rats fed E-dimethylaminoazobenzene. Cancer Res (7): 468-480, 1947. Baird WM: The use of radioactive Carcinogens to detect DNA modifications. In: Grover PL (ed) Chemical Carcinogens and DNA, Vol.

Comparison of arachidonic acid-dependent cooxidation to mixed-function oxidase-dependent cooxidation As stated earlier, a principal driving force for the study of peroxidatic xenobiotic oxidation is the fact that it might represent a pathway for metabolic activation that is distinct S6 from the well-studied mixed-function oxidase pathways. Let us examine the evidence that these are two distinct systems and compare the properties of both. 1. Proteins involved. Mixed-function oxidases require NADPH to trigger oxidation whereas PGH synthase-dependent cooxidation is triggered by the addition of arachidonic acid (35,72).

This oxidation may be related to the chemopreventive activity of retinoids or to their ability to act as tumor promoters under certain experimental conditions (70,71). 5. Comparison of arachidonic acid-dependent cooxidation to mixed-function oxidase-dependent cooxidation As stated earlier, a principal driving force for the study of peroxidatic xenobiotic oxidation is the fact that it might represent a pathway for metabolic activation that is distinct S6 from the well-studied mixed-function oxidase pathways.

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