Chemical Carcinogenesis and Mutagenesis I by H. C. Pitot (auth.), Colin S. Cooper Ph.D., Philip L. Grover

By H. C. Pitot (auth.), Colin S. Cooper Ph.D., Philip L. Grover D.Sc. (eds.)

I were privileged to witness and perform the nice progress of data on chemical carcinogenesis and mutagenesis for the reason that 1939 whilst I entered graduate university in biochemistry on the collage of Wisconsin­ Madison. I instantly began to paintings with the carcinogenic aminoazo dyes un­ der the path of Professor CARL BAUMANN. In 1942 I joined a fellow graduate pupil, ELIZABE1H CAVERT, in marriage and we quickly started a joyous half­ nership in study on chemical carcinogenesis on the McArdle Laboratory for melanoma examine within the collage of Wisconsin scientific tuition in Madison. This collaboration lasted forty five years. i'm very thankful that this quantity is dedi­ cated to the reminiscence of Elizabeth. the $64000 and sundry issues which are reviewed right here attest to the ongoing progress of the fields of chemical automobile­ cinogenesis and mutagenesis, together with their contemporary and fruitful union with viral oncology. i believe very positive in regards to the software of data in those fields to the eventual answer of various difficulties, together with the detection and estimation of the dangers to people of environmental chemical cancer causing agents and re­ lated factors.

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1984). Since this enzyme tends to inhibit the formation of free radicals during normal metabolic reactions, it is quite likely that these antioxidants exert their effect through inducing the activity of this enzyme. Therefore, the exact mechanism whereby antioxidants alter the process of carcinogenesis is not clear, but it is likely that various mechanisms are involved, some of which probably affect the formation of free radicals by chemical carcinogens, other xenobiotics, and normal metabolic pathways.

C. PITOT Glauert HP, Schwarz M, Pitot HC (1986) The phenotypic stability of altered hepatic foci: effect of the short-term withdrawal of phenobarbital and of the long-term feeding of purified diets after the withdrawal of phenobarbital. Carcinogenesis 7: 117-121 Goelz SE, Vogel stein B, Hamilton SR, Feinberg AP (1985) Hypomethylation of DNA from benign and malignant human colon neoplasms. Science 228:187-190 Goldsworthy T, Campbell HA, Pitot HC (1984) The natural history and dose-response characteristics of enzyme-altered foci in rat liver following phenobarbital and diethylnitrosamine administration.

Similar activation of p-dimethylaminoazobenzene has also been reported (VASDEV et al. 1982). p-Naphthylamine (FISCHER and MASON 1986), benzidine (JOSEPHY et al. 1983), and 2-aminofluorene (KRAuss and ELING 1985) appear to undergo similar metabolic reactions or are capable of such reactions. Furthermore, the endoperoxidation of arachidonic acid is not the only pathway leading to the formation of free radical intermediates of chemical carcinogens, since peroxides of unsaturated fatty acids within membranes appear to be capable of carrying out similar chemical reactions (FwYD 1981; McNEILL and WILLS 1985).

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