Rate Of Lactic Acid Production Research Articles

Carbohydrate metabolism of schistosoma mansoni.

1. Schistosoma mansoni utilizes in 1 hour an amount of glucose equivalent to one-sixth to one-fifth of its dry weight. Over 80 per cent of the metabolized glucose is converted to lactic acid by this organism. 2. The rates of glucose utilization and of lactic acid production by S. mansoni are the same under aerobic and under anaerobic conditions. 3. A high rate of lactic acid production and the absence of a postanaerobic increase in the oxygen uptake differentiate S. mansoni from most other parasitic helminths whose metabolism has been studied. 4. Arsenite and p-chloromercuric benzoate inhibit in low concentrations the oxygen uptake and the rate of glycolysis of S. mansoni. This inhibition is not prevented or reversed by an excess of glutathione or of thioglycollate. 5. Fluoride inhibits the removal of glucose and the production of lactic acid by S. mansoni to the same degree. 6. Low concentrations of quinacrine (atabrine) do not affect the respiration or the carbohydrate metabolism of the schistosomes. 7. The inhibitory effect of aldehydes on the metabolism of S. mansoni has been measured. Among this group of compounds dl-glyceraldehyde and o-nitrobenzaldehyde are the most effective inhibitors of glycolysis. 8. In a concentration of 2.6 x 10(-6)M (1:1,000,000) a cyanine dye inhibits almost completely the respiration of the schistosomes, but has no effect on their rate of glycolysis. The oxygen uptake of the worms is inhibited by fuadin to a greater degree than their rate of glycolysis. 2-methyl-1,4-napthoquinone is a much more effective inhibitor of glycolysis than of the respiration of S. mansoni. The latter compound interacts with plasma albumin and, therefore, its inhibitory action on the metabolism of the schistosomes is greatly reduced in human serum or plasma. 9. Evidence is discussed which indicates that, in contrast to glycolysis, respiratory metabolism is not essential for the survival of S. mansoni.

STUDIES ON THE METABOLISM OF THE FILARIAL WORM, LITOMOSOIDES CARINII

The filarial worm, Litomosoides carinii, has a high rate of aerobic and anaerobic glucose metabolism. Aerobically 30 to 45 per cent of the glucose utilized was converted to lactic acid, 25 to 35 per cent to acetic acid, and 10 to 20 per cent to a polysaccharide. Anaerobically over 80 per cent of the total carbohydrate removed by the filariae was metabolized to lactic acid, the remainder was accounted for by the production of acetic acid. The high rates of aerobic and anaerobic lactic acid production and of aerobic polysaccharide synthesis, as well as the absence of a postanaerobic increase of the oxygen uptake, differentiate the filarial worm, L. carinii, from the known metabolic characteristics of all other helminths and of most other invertebrates. The rate of aerobic lactate and pyruvate utilization by the filariae appears to be much slower than that of glucose. Anaerobically, dismutation of two moles of pyruvate to one mole of lactate, one mole of acetate, and one mole of CO(2), occurred. Aerobically, acetate production from pyruvate exceeded that of lactate. A significant proportion of the pyruvate metabolized aerobically by the filariae was not oxidized to acetate. In the presence of fluoroacetate, aerobic incubation of the filariae in a glucose-containing medium produced a marked decrease in the respiration of the organisms, an accumulation of pyruvate, a decreased formation of acetate, and an increase in aerobic glycolysis. Low concentrations of fluoroacetate (1 x 10(-3)M) inhibited the oxidative metabolism of pyruvate which did not result in the conversion of pyruvate to acetate; higher concentrations of this inhibitor produced also a decreased oxidation of pyruvate to acetate. No evidence has been obtained that fluoroacetate inhibits the respiration of the filariae because of a competitive inhibition of acetate oxidation. Respiration and glycolysis of filariae were markedly decreased by low concentrations of p-chloromercuric benzoate. This inhibition could not be reversed by a large excess of thioglycollate, cystein, glutathione, or H(2)S. Respiration of the filariae was completely inhibited by cyanide (2 x 10(-4)M). The cyanine dyes, a group of compounds possessing high chemotherapeutic activity in filariasis of the cotton rat, inhibited in low concentrations (6.5 x 10(-8)M) the oxygen uptake of the filarial worms. This decrease in oxidative metabolism was associated with a compensatory increase in aerobic glycolysis of the worms and with decreased rates of acetate production and of polysaccharide synthesis. The same metabolic changes were observed in filariae removed from cotton rats to which subcurative doses of a cyanine dye had been administered. Concentrations of cyanine dyes which produced an almost complete inhibition of filarial respiration had no effect on the rate of anaerobic glycolysis of the worms nor on the activity of cytochrome C or of cytochrome oxidase. It is concluded that, in contrast to many other parasitic invertebrates, oxidative metabolism is essential for the survival of the filarial worm, L. carinii, and that the chemotherapeutic activity of the cyanine dyes in filariasis of the cotton rat is due to the inhibitory effect of this group of compounds on the respiratory metabolism of the parasite.

Post-mortem breakdown of glycogen and accumulation of lactic acid in fish muscle.―I

Following the work of Macleod and Simpson (1927) and Leim, Macleod, and Simpson (1927), Maopherson (1932) studied tire post-mortem changes in glycogen, free sugar, and lactic acid occurring in haddock muscle during storage at 0°C. It was found that glycogen disappeared far more rapidly than lactic acid accumulated without any change taking place in tire free-sugar value, and the concentration of lactic acid at its maximum was never more than equivalent to two-thirds of the glycogen loss. Efforts to show tire accumulation of certain possible intermediate substances (dextrin, trisaccharide) gave negative results. The present study was carried out in a similar manner to that of Smith (1929), attention doing paid to the effect of temperature on rate of change rather than to the actual relation between glycogen breakdown and lactic acid accumulation during storage after death. In frog's muscle Smith showed that during storage at low temperatures, the rate of lactic acid accumulation passed through a maximum at —2-5°C ., and thereafter decreased as the temperature of storage was lowered, until at —10°C. no accumulation of lactic acid took place. Further, a "critical" temperature of freezing occurred at —1 - 6°C. In muscle stored for 24 hours at any freezing temperature above —1-6°C., then thawed to 5°C ., the lactic acid which had accumulated in the frozen state disappeared until the normal resting level of 0.0 5% was reached. Muscle stored for 24 hours at temperatures below —1 -6°C. showed on tharwing to 5°C. further accumulation of acid until the rigor maximum was reached. Storage of frog's muscle therefore for 24 hours at trooping temperatures of —1.6°C. and below —1.6°C. caused irretrievable damage to the lactic acid recovery mechanism. In this paper results are given of a general survey of the effect of temperature on the rates of glycogenolysis and lactic acid production in fish muscle. It was found that as in frog's muscle the rate of change passes through a maximum at some temperature between 0° and —10°C.

Effect of Sodium Fluoride on Lactic Acid Production by Strepto-bacterium Casei

Fluorides, like the halogenated acetic acids, inhibit the formation of lactic acid from hexose or glycogen in biological systems by causing the formation of stable hexose esters. We have reported observations on the course of iodoacetate poisoning in Streptobacterium casei, and can now add to these the course of events in fluoride poisoning. The experimental procedure was the same as previously reported except that various concentrations of sodium fluoride instead of iodoacetate, made up in the suspension medium, were placed in the sidearms of the Warburg vessels. As in iodoacetate poisoning there was a brief latent period on addition of fluoride. However, the rest of the picture was quite different. Whereas inhibition was observed in all cases with iodoacetate, in concentrations ranging from 0.0004% to 4.0%, with fluoride we found that concentrations up to 0.08% actually stimulated lactic acid production. At a concentration of 0.10%, the lactic acid-time curve was approximately the same as that of the control. Increasing the fluoride concentration up to 0.18% caused small decreases in the rate of lactic acid production, then there was a sharp decrease in this rate when the fluoride concentration reached 0.20%. Little more inhibition resulted from a fluoride concentration up to 0.5%. Unlike the smooth continuous decrease in rates observed with iodoacetate, fluoride poisoning causes a rather sharp break in the rate of lactic acid production, after which the rate remains constant for several hours, at a characteristic value for each fluoride concentration. As in previous experiments, lactic acid production in the control vessels was carried out at a constant rate for some 7 hours, the duration of the experiments.

Influence of the Concentration of Iodoacetic Acid Upon Excitability and Chemical Changes in Muscle

1. There is conclusive evidence that iotloacetic acid slows the rate of lactic acid production in the anaerobic recovery period, and the slowing is in proportion to the concentration of the poison. 2. Iodoacetic acid does not accelerate removal of lactate under anaerobic conditions.