Download Organ and Species Specificity in Chemical Carcinogenesis by Jerry M. Rice, Charles H. Frith (auth.), Robert Langenbach, PDF

By Jerry M. Rice, Charles H. Frith (auth.), Robert Langenbach, Stephen Nesnow, Jerry M. Rice (eds.)

The Symposium on Organ and Species Specificity in Chemical Carcinogenesis used to be held March 1981 in Raleigh, North Carolina. Dr. James Miller concluded this Symposium with those feedback: "Without a doubt we all could agree this has been a really winning symposium in illustrating a really wide selection of chemical, stereochemical, biochemical, metabolic, molecular, and organic elements in chemical carcinogenesis. i believe it truly is noteworthy that some of the discussions have handled pharmacodynamic, or toxicodynamic, components which could impression the organic actions of the tremendous wide selection of buildings that we elect to name chemical cancer causing agents. I clearly desire that once this symposium every person right here will observe the very nice desire we have now for extra details on those brokers within the species we profess to be operating for, the human species. We badly want an sufficient facts base on human organs, human tissues, human cells, human subcellular arrangements, and human physique fluids. i don't believe we will depend on extrapolations of information on chemical carcinogenesis from experimental animals to people, irrespective of how subtle or believable those extrapolations could seem, till we all know way more approximately chemical carcinogenesis in people. Now, i would wish to upload a slightly own be aware. As a lot of you recognize, my spouse and i've shared a joint profession of a few forty years during this box, and i might wish to emphasize in those ultimate feedback the issue of youth.

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Sample text

The physiology of these species is obviously quite different, and this difference is reflected in the kinetic patterns of AFBl adducts formed in DNA after a single dose of AFB1. In rat liver DNA was rapidly modified by AFBl (see Figure 3). The maximum level of AFBl products occurred at or slightly before 2 h after injection of a sin~le subacute dose. 5 h (21). This lesion initially represented 80% of covalent products formed in DNA. Its rapid disappearance was due to removal from DNA and conversion to imidazole ring-opened products.

M. RICE AND C. H. : If you supplement your histologic evaluation with biochemical markers, can you improve the accuracy and efficiency of your microscopic examination? Could you bridge the gaps that exist between gross identification and microscopic diagnosis by using biochemical markers? : I think in some instances we could but I don't think that we would be completely successful. Jerry, do you want to comment on that? : The issue is still one of finding the lesion. While a biochemical marker can be extremely useful, still if the lesion is not seen and the piece of tissue that contains it is not taken, the biochemistry will be no better than the histologic preparation.

The qualitative distribution of hydrolyzed AFBl products was essentially identical to that found in the rat liver. The major products were AFB1-N7-GUA and the two products formed by scission of its imidazole ring. Minor adducts formed between AFMl and AFPl with guanine also were present. In contrast to the rat, the levels of these products in embryo DNA increased continuously during the 24-h period after exposure and decreased slowly during the next 48 h. Whether this decrease is due to adduct removal or increased DNA content of the embryo has not been determined.

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