scholarly journals Peroxisomal fatty acid oxidation as detected by H2O2 production in intact perfused rat liver

1981 ◽  
Vol 196 (3) ◽  
pp. 705-712 ◽  
Author(s):  
E C Foerster ◽  
T Fährenkemper ◽  
U Rabe ◽  
P Graf ◽  
H Sies
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Rat Liver ◽  
Hydrogen Donor ◽  
High Yield ◽  
Acid Oxidation ◽  
Isolated Perfused Rat Liver ◽  
H2o2 Production ◽  
Perfused Rat Liver ◽  
H2o2 Formation

1. H2O2 formation associated with the metabolism of added fatty acids was quantitatively determined in isolated haemoglobin-free perfused rat liver (non-recirculating system) by two different methods. 2. Organ spectrophotometry of catalase Compound I [Sies & Chance (1970) FEBS Lett. 11, 172-176] was used to detect H2O2 formation (a) by steady-state titration with added hydrogen donor, methanol or (b) by comparison of fatty-acid responses with those of the calibration compound, urate. 3. In the use of the peroxidatic reaction of catalase, [14C]methanol was added as hydrogen donor at an optimal concentration of 1 mM in the presence of 0.2 mM-L-methionine, and 14CO2 production rates were determined. 4. Results obtained by the different methods were similar. 5. The yield of H2O2 formation, expressed as the rate of H2O2 formation in relation to the rate of fatty-acid supply, was less than 1.0 in all cases, indicating that, regardless of chain length, less than one acetyl unit was formed per mol of added fatty acid by the peroxisomal system. In particular, the standard substrate used with isolated peroxisomal preparations (C16:0 fatty acid) gave low yield (close to zero). Long-chain monounsaturated fatty acids exhibit a relatively high yield of H2O2 formation. 6. The hypolipidaemic agent bezafibrate led to slightly increased yields for most of the acids tested, but the yield with oleate was decreased to one-half the original yield. 7. It is concluded that in the intact isolated perfused rat liver the assayable capacity for peroxisomal beta-oxidation is used to only a minor degree. However, the observed rates of H2O2 production with fatty acids can account for a considerable share of the endogenous H2O2 production found in the intact animal.

scholarly journals Influence of Kynurenate on Cholesterol and Fatty Acid Synthesis in Isolated Perfused Rat Liver

1973 ◽  
Vol 248 (2) ◽  
pp. 738-739
Author(s):  
Christian A. Barth ◽  
H. Jürgen Hackenschmidt ◽  
Elmar E. Weis ◽  
Karl F.A. Decker
Keyword(s):  
Fatty Acid ◽  
Rat Liver ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver

scholarly journals Endogenous hydroperoxide formation, cell volume and cellular K+ balance in perfused rat liver

1993 ◽  
Vol 296 (3) ◽  
pp. 701-707 ◽  
Author(s):  
N Saha ◽  
R Schreiber ◽  
S vom Dahl ◽  
F Lang ◽  
W Gerok ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Rat Liver ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Liver Mass ◽  
Hydroperoxide Formation ◽  
Close Relationship ◽  
H2o2 Formation ◽  
Net Release ◽  
K Release

Addition of benzylamine (0.5 mM) to isolated perfused rat liver led to a net release of K+ of 10.5 +/- 0.3 mumol/g, which was accompanied by a decrease in liver mass by 9.3 +/- 0.4% and a decrease of the intracellular water space by 13.7 +/- 0.6%, suggestive of hepatocellular shrinkage. Benzylamine had no effect on the perfusion pressure, and there was a close relationship between benzylamine-induced net K+ release and the accompanying decrease in liver mass. Benzylamine-induced net K+ release was sensitive to inhibition of monoamine oxidase by pargyline and increased with benzylamine flux through monoamine oxidase, suggesting its dependence on intracellular H2O2 formation. In line with this, infusion of H2O2 (but not of benzaldehyde, the other product of benzylamine metabolism) stimulated net K+ release from the liver. However, at a given H2O2 load K+ release was about 2-3-fold higher when H2O2 was generated intracellularly during the oxidation of benzylamine, as compared with exogenously delivered H2O2. Inhibition of catalase by 3-amino-1,2,4-triazole (0.2 mM) significantly increased the benzylamine-induced net K+ release as well as the benzylamine-induced release of GSSG into bile, but had no effect on benzylamine oxidation at monoamine oxidase. In the presence of Ba2+ (1 mM) or in Ca(2+)-free perfusions, the benzylamine-induced net K+ efflux was diminished by 60-70% or about 30%, respectively. This was not explained by the 20-30% decrease in flux through monoamine oxidase observed under these conditions. The results suggest that metabolic generation of H2O2 inside the liver leads to a net K+ efflux and subsequent hepatocellular shrinkage. Net K+ efflux under these conditions is enhanced when catalase is inhibited, suggesting that the rate of both intracellular H2O2 generation and degradation can modulate cellular K+ balance and cellular volume. The data support the idea that oxidative stress may affect hepatocellular functions also by lowering the hepatocellular hydration state.

scholarly journals Rates of ketone-body formation in the perfused rat liver

1969 ◽  
Vol 112 (5) ◽  
pp. 595-600 ◽  
Author(s):  
H. A. Krebs ◽  
Patricia G. Wallace ◽  
R. Hems ◽  
R. A. Freedland
Keyword(s):  
Fatty Acids ◽  
Rat Liver ◽  
Ketone Bodies ◽  
Short Chain Fatty Acids ◽  
Diabetic Rats ◽  
Isolated Perfused Rat Liver ◽  
Perfused Liver ◽  
Perfused Rat Liver ◽  
Normal Range ◽  
Physiological Value

1. The rates of formation of acetoacetate and β-hydroxybutyrate by the isolated perfused rat liver were measured under various conditions. 2. The rates found after addition of butyrate, octanoate, oleate and linoleate were about 100μmoles/hr./g. wet wt. in the liver of starved rats. These rates are much higher than those found with rat liver slices. 3. The differences between the rates given by slices and by the perfused organ were much higher with the long-chain than with short-chain fatty acids. The increments caused by oleate and linoleate were 12 and 16 times as large in the perfused organ as in the slices, whereas the increments caused by butyrate and octanoate were about four times as large. 4. The rates of ketogenesis in the unsupplemented perfused liver of well-fed rats, and the increments caused by the addition of fatty acids, were about half of those in the liver from starved rats. 5. The value of the [β-hydroxybutyrate]/[acetoacetate] ratio of the medium was raised by octanoate, oleate and linoleate. 6. Carnitine did not significantly accelerate ketogenesis from fatty acids. 7. Oleate formed up to 82% of the expected yield of ketone bodies. 8. In the liver of alloxan-diabetic rats the endogenous rates of ketogenesis were raised, in some cases as high as in the liver from starved rats, after addition of oleate. 9. On addition of either β-hydroxybutyrate or acetoacetate to the perfusion medium the liver gradually adjusted the [β-hydroxybutyrate]/[acetoacetate] ratio towards the normal range. 10. The [β-hydroxybutyrate]/[acetoacetate] ratio of the medium was about 0·4 when slices were incubated, but near the physiological value of 2 when the liver was perfused. 11. The experiments demonstrate that for the study of ketogenesis slices are in many ways grossly inferior to the perfused liver.

Release and uptake of triglycerides by isolated perfused rat liver

1962 ◽  
Vol 202 (2) ◽  
pp. 353-358 ◽  
Author(s):  
Murray Heimberg ◽  
Ira Weinstein ◽  
Howard Klausner ◽  
M. L. Watkins
Keyword(s):  
Fatty Acid ◽  
Rat Liver ◽  
Nonesterified Fatty Acid ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Rapid Process ◽  
Fat Emulsions ◽  
Net Uptake ◽  
Uptake And Release

The uptake of triglycerides by the isolated perfused rat liver from synthetic neutral fat emulsions or from washed rat chylomicrons was investigated. It was observed that the uptake of triglycerides was more rapid in livers from starved rats than from normal fed animals. In the absence of added lipid to the perfusate, there was release of triglyceride from livers of fed animals, whereas there was a net uptake of endogenous perfusate triglyceride by livers from fasting rats. The data suggest that both uptake and release of triglyceride by liver occur simultaneously. In livers from fasted animals uptake may be the more rapid process, whereas in livers from fed rats both uptake and release may occur at more equal rates. In contrast to the triglycerides, no difference in rate of uptake of endogenous serum nonesterified fatty acid or of added fatty acid-albumin complex was observed with livers from either fed or fasting animals.

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