Chris Carruthers

Antigenic Differences between Normal Mouse Epidermis and Methylcholanthrene-Induced Squamous-Cell Carcinomas

IgG preparations were made from antisera raised against the urea- and alkali-extracted antigens of normal mouse epidermis and methyl- cholanthrene-induced squamous-cell carcinomas. Immunodiffusion in

Differences in the Urea-Extracted or Fibrous Proteins of Mouse Epidermis at Various Stages of Malignant Transformation

The urea-extractable proteins of normal and hyperplastic mouse epidermis, papilloma, and squamous-cell carcinoma were fractionated by gel filtration on Sepharose 4B to yield proteins which were excluded and retarded. The level of the proteins which were excluded decreased from normal epidermis through hyperplastic epidermis, papilloma, and carcinoma, whereas the retarded protein fractions increased proportionately. Ultra-centrifugation of these urea proteins resulted in gel and supernatant fractions, each of which accounted for approximately 50% of the total proteins for normal epidermis, papilloma, and carcinoma. The gel and supernatant fractions and the proteins which were excluded and retarded by Sepharose 4B were employed in immunodiffusion in agar against antisera or IgG fractions of antisera raised against the various urea proteins. These results showed that antigenic differences existed between the fibrous proteins of normal epidermis and papilloma or carcinoma, but the latter two tissues were antigenically similar with respect to these proteins.

Effect of 12–O-Tetradecanoyl-Phorbol-13-Acetate and 3-Methylcholanthrene on the Toxicity of Nicotine Applied to Mouse Skin

The effect of the tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and 3-methylcholanthrene (MCA) on the toxicity of nicotine and the content of this alkaloid in mouse skin has been determined following the application of these reagents to the skin. TPA or MCA was applied to mouse skin at time 0, and then at various time intervals thereafter, nicotine was applied to the skin. The content of this alkaloid (nicotine DNA ratio) remaining in the skin was then determined 1/2 h after its application. After the application of TPA, the nicotine DNA ratio of the skin decreased from 120 at 1.8 h to 80 at 18 h, increased sharply from 24 h, reaching a maximum of 165 at 72 h, and then decreased gradually. As the nicotine DNA ratio of the skin increased, the mortality rate of the mice also increased, reaching a maximum of over 40% at 48 and 72 h following the application of TPA. When MCA was applied to mouse skin in the same fashion and then nicotine, there was a decrease in the nicotine DNA ratio similar to that induced by TPA and nicotine followed by an average increase in the nicotine DNA ratio of 130 at 72, 96 and 120 h. The mortality rate of these mice was low. Finally, ethyl phenyl propiolate (EPP) was applied to mouse skin at time 0, and nicotine was applied 24, 48, 72, 96 and 120 h later. The mortality rate was also quite low at these times 1/2 h after application of nicotine (nicotine was not determined in the skin). TPA has induced some change in the skin 24, 48, 72 and 96 h after its application which resulted in an increase in the toxicity of nicotine to mice. Nicotine was not detected by the gas chromatographic method employed in the serum or plasma of nicotine-treated and TPA and nicotine-treated mice even though the mice showed acute reactions of nicotine toxicity and the skin surface contained ample amounts of this alkaloid.

Ligandin Content of Normal and Carcinogen-Treated Rat Tissues

Ligandin was detected by immunofluorescence in tissue sections and determined by immunoquantitation in the cytosols of the liver, kidney and testes of normal and carcinogen-treated rats. Ligandin was not detected by either of these procedures in normal or carcinogen-treated rat lung, spleen, brain, and skeletal or cardiac muscle.