VOLUME 28 NUMBER 2 March 1966
On The Newer Method for Direct Measurement of Heart Movement in Animals
ZENGO KANDA, ATUSHI SEKIYA and MITSUYOSHI NAKASHIMA
pg(s) 101 - 109
Clinico-Biochemical Study on Senile Osteoporosis
MASASHI NAKAGAWA, REISUKE NATSUME, TOHRU YOSHIDA, MITSUNOBU SHIONO, OSAMU KIDA, HISASHI IWATA, HISASHI HIRAKOH and KEIICHI KASAHARA
pg(s) 110 - 125
A Stereotaxic Apparatus for Brain Surgery and High Frequency Coagulator with Automatic Thermocontrol
KENICHIRO SUGITA and KEIICHI MURATA
pg(s) 126 - 141
Effects of Irradiation on Cancer Toxin in Tumor-Bearing Hosts
SHOJI SUGA
pg(s) 142 - 161
Irradiation effects on cancer toxin, "toxohormone", in tumor-bearing hosts were investigated.
Crude toxohormone fractions were prepared from preoperatively co60-irradiated human gastric cancer by the method of Yunoki and Griffin.
1) It was demonstrated that Co60-irradiation reduced the liver catalase de- pressing action of the crude toxohormone fractions, but the yield of the fractions was less markedly affected.
2) Amberlite XE-64 column chromatography of the fractions revealed the decreased amount of the TH2 fraction which was reported to possess the most potent catalase depressing action.
3) Histological observations of the Co60-irradiated cancer were: a) focal necrosis and/or fibrosis of the tissue; b) degenerative changes of cancer cells, which varied in severity. Irradiation effects on cancer toxin were then investigated in connection with the tumor growth, using mice bearing a diploid Ehrlich ascites tumor.
1) In tumor-bearing mice, a decrease in liver catalase activity was observed 10 hours after irradiation with 200 or 500 r of X-rays. This decrease was ascribed to an enhanced release of the cancer toxin from the irradiated tumor cells.
2) After 500 r, the arrest of cell division occurred, whereas the average cell volume continued to increase. This increase in volume might be due to an in- crease in new cell substance. On the other hand, the estimations of liver catalase activity demonstrated an increase in activity 48 hours after irradiation.
3) This later increase in liver catalase activity was also observed frequently after exposure to 200 r. Such irradiation effect was, however, diminished by the concomitant administration of a radioprotective agent, cysteine. On the other hand, no influence of cysteine was observed with regard to the early decrease in liver catalase activity. From these findings, the later increase in liver catalase activity was most likely interpreted to be due to the lowered amount of the cancer toxin after irradiation, which was resulted from a decreased synthesis denovo of the toxin. In other words, there was a possible relation of the radiosensitive enzymes with the synthesis of the cancer toxin by the tumor cells.
Crude toxohormone fractions were prepared from preoperatively co60-irradiated human gastric cancer by the method of Yunoki and Griffin.
1) It was demonstrated that Co60-irradiation reduced the liver catalase de- pressing action of the crude toxohormone fractions, but the yield of the fractions was less markedly affected.
2) Amberlite XE-64 column chromatography of the fractions revealed the decreased amount of the TH2 fraction which was reported to possess the most potent catalase depressing action.
3) Histological observations of the Co60-irradiated cancer were: a) focal necrosis and/or fibrosis of the tissue; b) degenerative changes of cancer cells, which varied in severity. Irradiation effects on cancer toxin were then investigated in connection with the tumor growth, using mice bearing a diploid Ehrlich ascites tumor.
1) In tumor-bearing mice, a decrease in liver catalase activity was observed 10 hours after irradiation with 200 or 500 r of X-rays. This decrease was ascribed to an enhanced release of the cancer toxin from the irradiated tumor cells.
2) After 500 r, the arrest of cell division occurred, whereas the average cell volume continued to increase. This increase in volume might be due to an in- crease in new cell substance. On the other hand, the estimations of liver catalase activity demonstrated an increase in activity 48 hours after irradiation.
3) This later increase in liver catalase activity was also observed frequently after exposure to 200 r. Such irradiation effect was, however, diminished by the concomitant administration of a radioprotective agent, cysteine. On the other hand, no influence of cysteine was observed with regard to the early decrease in liver catalase activity. From these findings, the later increase in liver catalase activity was most likely interpreted to be due to the lowered amount of the cancer toxin after irradiation, which was resulted from a decreased synthesis denovo of the toxin. In other words, there was a possible relation of the radiosensitive enzymes with the synthesis of the cancer toxin by the tumor cells.