에르릿히 복수종양에 있어서 젖산 각 탄소산화과정의 분해 경로에 관한 연구

Abstract

Metabolic pathway of carbon atoms of lactate in the Ehrlich ascites tumor tissue homogenate was observed in mice by means of labeled lactate. Tumor tissue homogenates were incubated in medium containing either one of CIL1, C1L2, or C14-3-lactate. Lactate concentration in incubation medium was maintained at 50 mg%. At the end of incubation period, gas sample and incubation medium were analyzed for total CO2 production rate, radio-activities of respiratory CO2 produced , lactate uptake rate and pyruvate appearance rate. The following results were obtained. 1. Mean value of lactate uptake rate was 2.07 μM/ hr/gm and pyruvate appearance rate was 0.039 μM/ hr/gm. The mean value of total CO2 production rate was 15.1 μM/hr/gm. These values showed no difference regardless of the shift of labeling position of lactate carbon atom. 2. Respiratory C140 2 yield from OLI-lactate incubation medium was 14.4% of the total CO2production rate and this proportion was larger than that of from 0'-2 and OL3-lactate media. 0'02 yield from OL2 and 0'-3-lactate media were 0.74 and 0.65 % of the total CO2 production rate, respectively. This shows that carboxyl carbon of lactate contributes a larger proportion in producing respiratory CO2 than a and ~ carbons of lactate. 3. The fraction of disappeared lactate from incubation medium into respiratory CO: was expressed as re lative lactate disappearance rate into CO2 (RLDc02) and was averaged 38.3%. Relative lactate disappearance rate into pyruvate (RLDpy) was 1. 9%. Therefore , about 40 % of disappeared lactate were accounted for by the conversion into respiratory CO2and pyruvate. It is concluded that in the catabolic pathway of lactate in ascites tumor tissue CO2 was easily produced from carboxyl carbon of lactate by oxidative decarbo' xylation as in the normal tissue , and further oxidation of 2 carbon unit via the TCA cycle was remarkably inhibited. On the other hand, from the fact there are little differences in 0'02 yield between 0'-2 and OL 3-lactate medium group, it is reasonable to assume that carbohydrate synthesis was also inhibited in the ascites tumor tissue. Possible explanations for these effects were briefly discussed.