[D(-)Lactic acid--a metabolism problem].

The metabolization of D-lactate was examined in volunteers by means of renal excretion after intake of DL-lactate, and in rats as well as in rat liver in vitro by the oxidation rate of 14C-D-lactate to 14CO2. In five volunteers after intake of DL-lactate containing 1.60 to 6.5 mmol D-lactate per kg 0.75 (equiv. to 50-200 mg/kg) an average of 1.2-2.2 percent of the dose was eliminated in urine. The exponential decline of renal elimination during the first 15 hours after intake and the total excretion time up to 24 hours (and possibly more) suggested a quite slow rate of metabolism. Following intraperitoneal injection of 2.0 and 4.2 mmol per kg 0.75 in rats (equiv. to 62 and 131 mg per kg in man) the oxidation rate of D-lactate vs. L-lactate was significantly and strongly reduced. After intragastral dosage of DL-lactate containing 4.2 to 12.8 mmol D-lactate per kg 0.75 an average of 0.9 and 2.4 percent were excreted in urine as D-lactate and as metabolites. Even after the lowest dose D-lactate oxidation to CO2 extended far beyond 8 hours. Higher doses decreased the rate of D-lactate oxidation. In tissue samples of rat liver in vitro oxalate, L-lactate and pyruvate inhibited the oxidation of D-lactate. L-lactate in a physiological concentration was sufficient to effect an inhibition of 20 percent. A significant increase of D-lactate oxidation with increasing body weight and a significantly higher oxidation of D-lactate in conventionals vs. germ-free rats indicated the influences of age and gastro-intestinal flora on D-lactate metabolism. From these results it is concluded that D-lactic acid is only slowly metabolized if the concentration of one or other of the lactate isomers is elevated.