scholarly journals Influence of some aliphatic alcohols on the metabolism of rat liver slices

1967 ◽  
Vol 105 (1) ◽  
pp. 93-97 ◽  
Author(s):  
Olof A. Forsander

The influence of some aliphatic alcohols on oxygen uptake, carbon dioxide production, acid formation and lactate and pyruvate concentrations of rat liver slices was studied. At the concentrations used, none of the alcohols was found to influence oxygen uptake. Of the alcohols that are not oxidized by liver alcohol dehydrogenase, methanol increased carbon dioxide production, propan-2-ol decreased it and 2-methylpropan-2-ol was without influence. All the alcohols that are oxidized by the enzyme strongly decreased carbon dioxide production. The alcohols that are not oxidized had no marked effect on the lactate/pyruvate concentration ratio, whereas the other alcohols strongly increased the ratio. A highly significant correlation was found between the effects of the alcohol on pyruvate concentration and carbon dioxide production. It is assumed that the shift in the redox potential inhibits the function of the tricarboxylic acid cycle of the liver.

1957 ◽  
Vol 35 (1) ◽  
pp. 103-111
Author(s):  
Jerrold G. Goldman ◽  
Arnold H. Schein ◽  
Bruce McKay

Oxygen uptake could not be demonstrated when uracil, uridine, or uridylic acid and various supplements were incubated with rat liver preparations. Attention was directed towards the likelihood that the initial step of uracil catabolism in mammals is a reduction such as occurs in yeasts. Various techniques were employed to measure the possible reduction of uracil to 4,5-dihydrouracil but no experimental evidence was uncovered that this latter compound was formed. While Canellakis has recently shown that the reaction uracil → 4,5-dihydrouracil does take place in mammalian tissues and that TRPH is required, this requirement must be specific since addition of DPNH in the experiments described below was without effect. A small fraction of the ureido carbon (C-2) of uracil-2-C14 was released as carbon dioxide by rat liver slices. None of the results obtained can be reconciled with the oxidative pathway for uracil catabolism in mammals proposed by Cerecedo.


1957 ◽  
Vol 35 (1) ◽  
pp. 103-111
Author(s):  
Jerrold G. Goldman ◽  
Arnold H. Schein ◽  
Bruce McKay

Oxygen uptake could not be demonstrated when uracil, uridine, or uridylic acid and various supplements were incubated with rat liver preparations. Attention was directed towards the likelihood that the initial step of uracil catabolism in mammals is a reduction such as occurs in yeasts. Various techniques were employed to measure the possible reduction of uracil to 4,5-dihydrouracil but no experimental evidence was uncovered that this latter compound was formed. While Canellakis has recently shown that the reaction uracil → 4,5-dihydrouracil does take place in mammalian tissues and that TRPH is required, this requirement must be specific since addition of DPNH in the experiments described below was without effect. A small fraction of the ureido carbon (C-2) of uracil-2-C14 was released as carbon dioxide by rat liver slices. None of the results obtained can be reconciled with the oxidative pathway for uracil catabolism in mammals proposed by Cerecedo.


1941 ◽  
Vol 140 (1) ◽  
pp. 285-291
Author(s):  
Harry D. Baernstein ◽  
J.A. Grand

1963 ◽  
Vol 41 (3) ◽  
pp. 793-803 ◽  
Author(s):  
Edward Majchrowicz ◽  
J. H. Quastel

Ethanol, at concentrations up to 3 mM, whilst having little inhibitory effect on the production of respiratory CO2of rat liver slices, has a marked suppressing action on the formation of labelled CO2from labelled glucose. The suppression of C14O2formation by ethanol from radioactive glucose is independent of the concentration of the latter and amounts to 57% with 3 mM ethanol after 1 hour's incubation. The results are consistent with the conclusion that ethanol gives rise more rapidly than glucose to acetyl CoA and that the large suppressing action of ethanol in rat liver slices is due to isotopic dilution of labelled acetyl CoA derived from the labelled sugars with the unlabelled acetyl CoA derived from ethanol. Ethanol exercises a larger inhibition of the rate of C14O2formation from glucose-6-C14than from glucose-1-C14. The difference between the effects of ethanol on C14O2formation from glucose-1-C14and glucose-6-C14is presumably due to operation of the hexosemonophosphate shunt.The higher aliphatic alcohols have about the same diminishing effect on C14O2formation from glucose-U-C14and fructose-U-C14as does ethanol. This observation may also be a consequence of dilution of labelled acetyl CoA derived from the sugars by unlabelled acetyl CoA coming from the added alcohol. Incorporation of radioactive carbon from the labelled sugars into liver proteins and lipids is inhibited by ethanol and higher aliphatic alcohols, and the inhibitions are similar in magnitude to those of C14O2formation. These may be accounted for by isotopic dilution. The amounts of C14incorporated into lipids and proteins from radioactive glucose and fructose are small, being about 1/10th of that appearing in the CO2.The higher aliphatic alcohols suppress total CO2formation during rat liver slice respiration much more than does ethanol at equivalent concentrations.


1965 ◽  
Vol 25 (2) ◽  
pp. 123-128 ◽  
Author(s):  
Nirmal Chakravarty

Glycolytic activity of rat peritoneal mast cells has been measured by the Cartesian ampulla diver technique. The rates of anaerobic glycolysis, expressed as CO2 expelled from a bicarbonate medium, are 1.70 x 10-6 µl and 1.43 x 10-6 µl per cell per hour with and without glucose, respectively. The aerobic glycolysis rate in the presence of glucose, assuming the respiratory quotient to be 1, is 0.93 x 10-6 µl CO2 per cell per hour. It is pointed out that the anaerobic and non-respiratory aerobic carbon dioxide production by mast cells is much higher than the respiratory oxygen uptake reported previously. These values have been interpreted in terms of glucose utilization.


1966 ◽  
Vol 44 (8) ◽  
pp. 1077-1086 ◽  
Author(s):  
E. W. B. Ward

Conventional manometric procedures were used to measure oxygen uptake and carbon dioxide evolution by cells of a low-temperature basidiomycete. Total respiration was lowest and, relatively, endogenous respiration was highest in old cells. During starvation, endogenous respiration decreased but did so most rapidly in young cells. Maximum response to exogenous glucose was obtained from young cells after starvation. The respiratory quotient of endogenous respiration fell from 1.0 to approximately 0.7 during starvation, indicating a change in endogenous substrate. Conversely the respiratory quotient for exogenous respiration of added glucose increased with the starvation period. The level of oxidative assimilation of glucose was shown to be high (80-90%) and evidence was obtained that exogenous glucose did not suppress endogenous respiration.The optimum temperature for oxygen uptake was 25 °C, below which the Q10 was approximately 2. At 30 °C the rate, while initially highest, decreased during the 6-hour incubation period.The fungus utilized various compounds as carbon sources, but not sucrose in short-term experiments. Glucose, but not xylose was fermented, although the ratio of carbon dioxide to ethanol was not 1:1. Inhibition by fluoride, arsenite, iodoacetate, fluoroacetate, and malonate suggested that both glucose and xylose are respired at least in part by the Embden-Meyerof pathway and the tricarboxylic acid cycle. Endogenous respiration was only slightly affected by these inhibitors.


2007 ◽  
Vol 13 (6) ◽  
pp. 462-469 ◽  
Author(s):  
Ross Arena ◽  
Jonathan Myers ◽  
Leon Hsu ◽  
Mary Ann Peberdy ◽  
Sherry Pinkstaff ◽  
...  

1944 ◽  
Vol 79 (1) ◽  
pp. 23-33 ◽  
Author(s):  
Jane A. Russell ◽  
C. N. H. Long ◽  
Alfred E. Wilhelmi

1. With increasing severity of shock following hemorrhage in fasted rats there is an increasing depression in the rate of oxygen uptake, in oxygen, of liver slices from the bled animals. The respiration of kidney tissue is only slightly depressed even in severe states of shock. 2. The rates of oxygen uptake of liver tissue from bled rats are nicely correlated with the increases in blood amino nitrogen that follow severe hemorrhage. 3. A supplement of coenzyme factors, in the form of a hot water extract of normal rat liver, increases the oxygen uptake of liver tissue from rats in mild shock, but is without effect on the respiration of liver slices from rats in moderate or severe shock. 4. The ability of rat liver to oxidize succinate is not impaired even in severe shock, but the extra oxygen uptake does not improve the basal rate of respiration of the tissue. 5. Effects on the rate of oxygen uptake of normal rat liver slices comparable to those seen after hemorrhage could be produced by exposing the tissue to an atmosphere of nitrogen for periods of 15 and 60 minutes. This treatment had more marked effects on the respiration of kidney slices than are found after hemorrhage, but the kidney, unlike the liver, exhibited a marked degree of recovery in the presence of glucose. 6. The significance of these findings is briefly discussed.


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