- 에르릿히 복수암에 있어서 C14-초산염 대사
- Metabolism of C14-acetate in the Ehrlich ascites tumor
- ㆍ 저자명
- 정원근(Chun, Won-Kun),이상돈(Rhee, Sang-Don)
- ㆍ 간행물명
- 대한생리학회지
- ㆍ 권/호정보
- 1970년|4권 2호(통권8호)|pp.25-32 (8 pages)
- ㆍ 발행정보
- 대한생리학회|한국
- ㆍ 파일정보
- 정기간행물|KOR| PDF텍스트(0.26MB)
- ㆍ 주제분야
- 의약학
Tissue homogenates of Ehrlich ascites tumor tissues and several normal tissue of mice were incubated separately in medium maintaining C14_acetate concentrations of 5, 10, 20, 30, 40, 50 and 60 mg%, in order to determine maximum oxidative rates of acetate. In every incubation experiments, respiratory CO2 samples rapped by alkaline which was placed in the center well of the incubation blask were analyzed for total CO2 Production rates and their radoactivies. The fractions of CO2 from medium acetate to total CO2 production rate were obtained with relative specific activities (RSA) which were calculated by ratio between specific activities (SA) of CO2 and medium C14_acetate and CO2 production rates from medium acetate were calculated from RSA and total CO2 production rates. Maximum plateau values of oxidative rates described above were determined at incubation experiments of various concentrations of medium acetate and compared the oxidative rates of acetate of tumor with those of normal tissues such as kidney, brain and liver. Maximum plateau values of total CO2 Production rates were obtained at acetate concentration of 20 mg% and represent 25.0±0.54 μM/hr/gm in the brain, 16.3±2.5 in the kidney, 9.1±1.78 in the liver and 11.5±3.2 μM/hr/gm in the ascites tuners. Substancial CO2 yield was observed in the tumor tissues as in the normal tissues. On the other hand, plateau values of RSA were 25.7±1.04% in thee brain, 9.1±0.72% in the kidney, 2.5±0.73% in the liver and 0.51±0.12% in the tumor tissues. CO2 yields from the medium acetate, were 4.19 in the kidney, 2.28 in the brain, 0.228 in the liter and 0.059 μM/hr/gm in the tumor tissue. These show wide range even in the normal tissue but remarkable decrease in the tumor tissue. This fact means that further oxidation of acetate was inhibited remarkably in the tumor tissue.