인체 각종 암조직에 있어서 젖산 각탄소의 산화과정

Oxidation of Each Carbon of Lactate in Various Cancer Tissues of Human

Tissue homogenates of 10 kinds of human cancer tissues were incubated in medium containing either one of C¹⁴-1, C¹⁴-2, or C¹⁴-3-lactate as a substrate in order to observe the oxidative pathway of lactate in cancer tissues. Lactate concentration in incubation medium was maintained at 50 mg%. At the end of incubation period, gas samples and incubation media were analyzed for total CO₂ production rates, radioactivities of respiratory CO₂, lactate uptake rates and pyruvate appearance rates. The following results were obtained. 1. Lactate uptake rates in all of cancer tissues examined were less than 2.5 μM/hr/gm and much lower than those in normal tissues. 2. In the 10 kind of human cancer tissues, total CO₂ production rates were less than 10 μM/hr/gm, in all cases. These lower values impressed that oxidative metabolism in tumor tissues generally inhibited as compared with that in normal tissue. On the other hand, fractions of CO₂ derived from lactate to total CO₂ production rates were less than 15% except one case These facts showed that oxidation of lactate into CO₂ was greatly inhibited in tumor tissues. 3. Respiratory CO₂ yields from C-1 carbon of lactate in various cancer tissues were mean of 77.7% of total CO₂ yield from lactate and CO₂ yields from C-2 and C-3 carbon of lactate were mean of 9.1% and 12.6% respectively. These facts showed that carboxyl carbon of lactate oxidized more easily than α and β carbon of lactate. 4. In 10 kinds of cancer tissues, fractions of disappeared lacteate from media into CO₂ and pyruvate, which expressed as RLD CO₂ and RLDpy respectively, were about 5% in except 3 cases and less than 3% except one case. These fact showed that almost of disappeared lactate from media were degraded into compounds other than CO₂ and pyruvate. From the above date, it was suggested that in the oxidative pathway of lactate in cancer tissues CO₂ was easily Produced from carboxyl carbon of lactate by oxidative decarboxylation as in the normal tissue, and further oxidation of 2 carbon unit via TCA cycle was inhibited.