Carcinogenesis by carbamic acid esters and their binding to DNA.
The tumor-initiating potency of three simple alkyl carbamates and mono-N-substituted ethyl carbamates was examined in Hall strain mice. The binding of 14C-labeled carbamates of DNA was measured in Crackenbush mice. Ethyl carbamate was the most potent carcinogen for the epidermis, liver, and lung, followed by its N-alkyl derivatives. Methyl carbamate was without effect but n-propyl and n-butyl were possible carcinogens. The ethyl esters bound to a greater extent to DNA in liver and skin than the methyl, n-propyl, and n-butyl esters and only this binding persisted. A preliminary application of croton oil increased the yield of skin tumors but not of liver or lung tumors. It also increased the binding of the alkyl carbamates to DNA in skin, the increase being greatest with ethyl carbamate. The binding persisted longer in treated than in non-croton oil-treated mice.
D000236:Adenoma / Q000139:chemically induced; D000818:Animals; D002219:Carbamates / Q000378:metabolism / Q000633:toxicity*; D006528:Carcinoma, Hepatocellular / Q000139:chemically induced; D003436:Croton Oil / Q000494:pharmacology; D004952:Esters; D006391:Hemangioma / Q000139:chemically induced; D007942:Leukemia, Experimental / Q000139:chemically induced; D008113:Liver Neoplasms / Q000139:chemically induced; D008175:Lung Neoplasms / Q000139:chemically induced; D008297:Male; D051379:Mice; D009374:Neoplasms, Experimental / Q000139:chemically induced*; D012878:Skin Neoplasms / Q000139:chemically induced
D002219:Carbamates; D004952:Esters; D003436:Croton Oil