Gann
Print ISSN : 0016-450X
Volume 43, Issue 4
Displaying 1-5 of 5 articles from this issue
  • SANJI KISHI, KATSUHIKO HARUNO
    1952 Volume 43 Issue 4 Pages 421-429
    Published: December 25, 1952
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    1) In albino rats fed on liver-carcinogenic diet containing DAB trend of the liver asparaginase activity was studied from early to later stages of experimental days, till developement of hepatoma.
    2) A few weeks after the experiment has been started, marked lowering of the liver asparaginase activity compared to that of normal was observed and this phenomenon was seen as long as DAB was added to the diet. Also in the later period, when the pathological changes of the liver occurred, the activity remained still very low.
    3) A group of rats was fed with DAB diet for a long period, thereafter addition of DAB was discontinued and was fed on normal diet for a while. Their liver asparaginase activity recovered nearly to normal, notwithstanding some pathological changes. In cases of hepatoma, on the contrary, the enzyme activity has never recovered.
    4) The asparaginase activity of hepatoma showed always the lowest value not only in the experiments where DAB feeding was discontinued, but also in those where DAB was given continuously.
    5) Activity of liver asparaginase in rats fed with normal diet added with beef liver powder for a few weeks showed extremely higher value than that of normal rats. In cases of the rats fed DAB and liver powder simultaneously, the activity was variable, though some of them were very high.
    6) In experiments with other azo dyes, OAT and AB were used besides DAB. In the early period of feeding the inhibiting actions of these azo dyes on the liver asparaginase activity were generally lower than that of DAB, which was most active among them.
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  • KAZUO MORI, SEIKO MOMOKI
    1952 Volume 43 Issue 4 Pages 431-436
    Published: December 25, 1952
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    It has been demonstrated that butter yellow feeding definitely reduces the liver catalase actvity in the course of liver cancer production. However, a further investigation showed that this reduction in the liver catalase activity becomes less marked when the animals are placed on normal diet after a difinite period of the dye feeding. Miller and his associates9, 10) have reported that the tissues of rats fed butter yellow contain more or less bound dye which decreases rapidly when the feeding of dye is stopped and there is no bound bye in the liver cancer and kidney. The difference in the liver catalase activity between dye fed and non-dye fed rats may be related intimately to the concentration of the dye in the tissues.
    It is noteworthy that in the liver cancer, however no difference in the catalase activity is to be seen between the rat fed diet with and without butter yellow.
    Also it was demonstrated that the kidney catalase tended to be unaffected or slightly higher than that of the corresponding controls during the butter yellow carcinogenesis.
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  • KAZUO MORI, SABURO KAWAI, YOSITERU SIGETA
    1952 Volume 43 Issue 4 Pages 437-441
    Published: December 25, 1952
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    The iron content of the liver of rats during the butter yellow (p-dimethylaminoazobenzene) carcinogenesis was determined. It was demonstrated that there was an initial elevation, which, however, decreased gradually proportional to hepatic changes. The peak of the iron content was at the early stage of the liver changes and the content was more than twice the normal. In the liver cancer, the iron content showed the lowest value which was only 58 per cent of normal.
    At the end of this paper it is pleasure to express our appreciation to Dr. S. Kishi for his kind advice on the experiment.
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  • KAZUO MORI
    1952 Volume 43 Issue 4 Pages 443-447_1
    Published: December 25, 1952
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Numerous investigators attempted to produce gastric lesions in the rat or mouse with various diets or chemicals, as presented in a comprehensive review by Sugiura.1)
    The criteria adopted in this paper for the gastric lesions of the forestomach were those of the rats which received tributyrin diet. In this laboratory, more than one hundred rats were fed for 500 days with the rice diet containing 5-10 per cent of butyric acid with a small amount of cod liver oil, supplemented with green vegetables just same as the above experiment. The results were almost similar to those obtained by Salmon and Copeland.2, 3) In the experiment, the amount of the butyric acid was reduced to the level of 5-10 per cant, less than half of the amount cited by Salmon, and few rats died during the early course of the experiment. And the stomachs of all rats fed for more than 50 days showed ulcers or small discrete papillomas. As indicated by Salmon, in the rats of this laboratory numerous cysts were found penetrating the muscularis mucosa, and these cysts were lined with stratified squamous epithelium and contained keratin in a lamellated fibrillary arrangement. These results of butyric acid feeding will be reported elsewhere.
    In the case of the rats fed acetic acid, no cyst or nodule containing keratin was demonstrated in the forestomach. But, except the absence of keratin cyst in the forestomach, the other gastric lesions caused by acetic acid were similar but less marked than those due to butyric acid.
    It is noteworthy that the two chemicals in the low fatty acid group similarly produce the gastric lesions of rats by oral administration. A question remaines as to how propionic acid, one of the low fatty acids, act on the forestomach of the rats, and the inverstigation is now under way in this laboratory.
    In conclusion the author wishes to express his sincere thanks to Dr. Sanji Kishi, Head of Biochemical Section of this School, for his valuable suggestions.
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  • KATSUO TAKEDA
    1952 Volume 43 Issue 4 Pages 449-480
    Published: December 25, 1952
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    It is necessary to select a suitable tumor and a pure strain of animals in order to study "the allergy and immunity against tumor."
    Fortunately we could find some pure strains of rats and a ascites tumor of rat (Yoshida sarcoma), being appropriate for the delicate observation on this study.
    During the successive transplantation of this tumor in rats we could learn the facts that the various attitude to Yoshida sarcoma among strains of rats, namely death of tumor (Yamashita strain etc.) and natural healing (Wistar strain etc.), is almost due to the genetical difference of strains between animal from which Yoshida sarcoma generated and animal in which this tumor was transplanted. The natural healing, followed by the vacuolar degeneration of tumor cells accompaning with the cell reaction and the fibrin exudation in abdominal cavity, occurs spontaneously after 8-12 days during proliferation of tumor cells, and it bases upon the interaction between immune body developed in animals against tumor cells during their growth and tumor cells as a antigen. When the proliferative activity of cells is weak and the development of immune body is strong, the natural healing occurs suddenly, while in inverse condition the animals die of tumor leaving no immunity. Therefore the correlative condition between proliferativity of tumor cells and the development of immune body exerts an important influence upon the death of tumor and the natural healing.
    The animals healed naturally from tumor inhibit the retransplantation of the same tumor in a long time (about 100 days), normal rat which were formerly inoculated with the sera of healed rats inhibit the transplantation of this tumor in a certain grade. This serum injured the sarcoma cells in a form of vacuolar degeneration in vitro, it agglutinated the tumor cells and it acted upon protein of tumor cells in the precipitin reaction and the complement fixation test. But the sera of rats died of tumor showed no activity in vitro, and even when these animals were immunized by means of intracutaneous transplanting and extraction by terns they showed no serum reaction, in spite of proving a certain resistance against retransplantation in these animals in a certain period.
    The sera of rabbit and goat immunized against Yoshida sarcoma showed a strong cytotoxic effect not only upon Yoshida sarcoma but also upon rats tissues (species specific immunity).
    When the sera were absorbed with erythrocytes of rat, there remained still more agglutinin against nucleated cell of rat and Yoshida sarcoma, just like as the sera of Wistar rat healed from Yoshida sarcoma. Being absorbed with emulsion of nucleated cells of rat or of killed Yoshida sarcoma, the sera showed no serum reaction against rat or tumor cells in vitro, but they had still injurious action upon Yoshida sarcoma in a certain grade in vitro and in vivo, just like as the immune sera of Yamashita rat against Yoshida sarcoma.
    When these immunized sera were absorbed sufficiently with raw Yoshida sarcoma, they showed no action not only upon rat but also upon tumor cells.
    Wistar rat immunized against normal tissues of Yamashita rat inhibit the transplantation of Yoshida sarcoma in a certain period and its serum showed a "taken" in the agglutination test against normal cells of Yamashita rat and also against Yoshida sarcoma in a slight grade. But when the sera were absorbed with normal cells of Yamashita strain it showed no action on both these normal and pathological cells in vitro or in vivo.
    Conclusively it is to say that the immunity against Yoshida sarcoma is partially depend upon the normal strain specificity between transplanted (immunized) rat strain and the strain from which Yoshida sarcoma generated. But there exists in sera still more an unkown factor which acts specifically upon Yoshida sarcoma.
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