Add time:07/27/2019         Source:sciencedirect.com

Present experimental approaches dealing with the mechanisms of carcinogenesis attempt to relate the known combinations of carcinogen with cellular macromolecules and the specific interaction necessary for the carcinogenic process. With this aim the effect of prefeeding a series of inhibitors of the hepatocarcinogenicity of N-2-fluorenyl-acetamide on the binding of agent to liver macromolecules was studied after a single intravenous injection of an active metabolic intermediate, n-hydroxy-n-2-fluoren-[9-14C]ylacetamide, into rats.Carcinogen binding to liver nuclear DNA was decreased appreciably by 4 weeks feeding of chloramphenicol, acetanilide, m-acetotoluidide, or indole, all of which were inhibitors of hepatocarcinogenesis. Feeding p-acetotoluidide, methionine, tyrosine, inosine, or guanine had no significant effect. Carcinogen binding to ribosomal RNA was decreased by indole, m- and p-acetotoluidide, l-tryptophan, guanine, or inosine. Increased binding to soluble RNA occurred after acetanilide and m- and p-acetoto-luidide. Chloramphenicol depressed, but indole, m- and p-acetotoluidide increased binding to microsomal proteins. Sliglit decreases in binding to soluble proteins occurred after Chloramphenicol, acetanilide, tryptophan and tyrosine, and increases after indole. m- and p-acetotoluidide.Only with respect to nuclear DNA was there a relationship between depressed binding of isotope from n-hydroxy-n-2-fluorenylacetamide after prefeeding select agents and the inhibitory effect of these agents on tumor induction in the liver of rats.

We also recommend Trading Suppliers and Manufacturers of 2'-HYDROXY-P-ACETOTOLUIDIDE, 98 (cas 13429-10-2). Pls Click Website Link as below: cas 13429-10-2 suppliers