Energy Metabolism Following Prolonged Hepatic Cold Preservation: Benefits of Interrupted Hypoxia on the Adenine Nucleotide Pool in Rat Liver

Cryobiology ◽  
1999 ◽  
Vol 39 (2) ◽  
pp. 130-137 ◽  
Author(s):  
S.J. Mitchell ◽  
T.A. Churchill ◽  
M.C. Winslet ◽  
B.J. Fuller
Keyword(s):  
Energy Metabolism ◽  
Rat Liver ◽  
Adenine Nucleotide ◽  
Cold Preservation ◽  
Adenine Nucleotide Pool

Early effects of phenobarbital on the adenine nucleotide pool of rat liver

1972 ◽  
Vol 21 (14) ◽  
pp. 1929-1934 ◽  
Author(s):  
Roy McCauley ◽  
John O'Neill ◽  
Daniel Couri
Keyword(s):  
Rat Liver ◽  
Adenine Nucleotide ◽  
Early Effects ◽  
Adenine Nucleotide Pool

Skeletal muscle myosin heavy chain isoforms and energy metabolism after clenbuterol treatment in the rat

2000 ◽  
Vol 279 (3) ◽  
pp. R1076-R1081 ◽  
Author(s):  
P. Rajab ◽  
J. Fox ◽  
S. Riaz ◽  
D. Tomlinson ◽  
D. Ball ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Myosin Heavy Chain ◽  
Body Mass ◽  
Heavy Chain ◽  
Adenine Nucleotide ◽  
Prolonged Treatment ◽  
Skeletal Muscle Myosin ◽  
Adenine Nucleotide Pool ◽  
Muscle Myosin

Prolonged treatment with the β2-adrenoceptor agonist clenbuterol (1–2 mg · kg body mass−1 · day −1) is known to induce the hypertrophy of fast-contracting fibers and the conversion of slow- to fast-contracting fibers. We investigated the effects of administering a lower dose of clenbuterol (250 μg · kg body mass−1 · day−1) on skeletal muscle myosin heavy chain (MyHC) protein isoform content and adenine nucleotide (ATP, ADP, and AMP) concentrations. Male Wistar rats were administered clenbuterol ( n = 8) or saline ( n = 6) subcutaneously for 8 wk, after which the extensor digitorum longus (EDL) and soleus muscles were removed. We demonstrated an increase of type IIa MyHC protein content in the soleus from ∼0.5% in controls to ∼18% after clenbuterol treatment ( P < 0.05), which was accompanied by an increase in the total adenine nucleotide pool (TAN; ∼19%, P < 0.05) and energy charge [E-C = (ATP + 0.5 ADP)/(ATP + ADP + AMP); ∼4%; P < 0.05]. In the EDL, a reduction in the content of the less prevalent type I MyHC protein from ∼3% in controls to 0% after clenbuterol treatment ( P < 0.05) occurred without any alterations in TAN and E-C. These findings demonstrate that the phenotypic changes previously observed in slow muscle after clenbuterol administration at 1–2 mg · kg body mass−1 · day−1 are also observed at a substantially lower dose and are paralleled by concomitant changes in cellular energy metabolism.

scholarly journals Alteration of adenine nucleotide pool in old rat liver and its normalization with ammonium succinate

FEBS Letters ◽  
1983 ◽  
Vol 159 (1-2) ◽  
pp. 259-261 ◽  
Author(s):  
Yu.G. Kaminsky ◽  
E.A. Kosenko ◽  
M.N. Kondrashova
Keyword(s):  
Rat Liver ◽  
Adenine Nucleotide ◽  
Ammonium Succinate ◽  
Adenine Nucleotide Pool

Hepatic preconditioning preserves energy metabolism during sustained ischemia

2000 ◽  
Vol 279 (1) ◽  
pp. G163-G171 ◽  
Author(s):  
C. Peralta ◽  
R. Bartrons ◽  
L. Riera ◽  
A. Manzano ◽  
C. Xaus ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
High Energy ◽  
Energetic Cost ◽  
Main Role ◽  
Adenylate Energy Charge ◽  
Glycogen Depletion ◽  
Adenine Nucleotide Pool

We evaluated the possibility that ischemic preconditioning could modify hepatic energy metabolism during ischemia. Accordingly, high-energy nucleotides and their degradation products, glycogen and glycolytic intermediates and regulatory metabolites, were compared between preconditioned and nonpreconditioned livers. Preconditioning preserved to a greater extent ATP, adenine nucleotide pool, and adenylate energy charge; the accumulation of adenine nucleosides and bases was much lower in preconditioned livers, thus reflecting slower adenine nucleotide degradation. These effects were associated with a decrease in glycogen depletion and reduced accumulation of hexose 6-phosphates and lactate. 6-Phosphofructo-2-kinase decreased in both groups, reducing the availability of fructose-2,6-bisphosphate. Preconditioning sustained metabolite concentration at higher levels although this was not correlated with an increased glycolytic rate, suggesting that adenine nucleotides and cAMP may play the main role in the modulation of glycolytic pathway. Preconditioning attenuated the rise in cAMP and limited the accumulation of hexose 6-phosphates and lactate, probably by reducing glycogen depletion. Our results suggest the induction of metabolic arrest and/or associated metabolic downregulation as energetic cost-saving mechanisms that could be induced by preconditioning.

Permeability transition in rat liver mitochondria is modulated by the ATP-Mg/Pi carrier

2003 ◽  
Vol 285 (2) ◽  
pp. G274-G281 ◽  
Author(s):  
Thilo Hagen ◽  
Christopher J. Lagace ◽  
Josephine S. Modica-Napolitano ◽  
June R. Aprille
Keyword(s):  
Rat Liver ◽  
Mitochondrial Permeability Transition ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Permeability Transition ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Mitochondrial Permeability ◽  
Nucleotide Content ◽  
Adenine Nucleotide Pool

Mitochondrial permeability transition, due to opening of the permeability transition pore (PTP), is triggered by Ca2+ in conjunction with an inducing agent such as phosphate. However, incubation of rat liver mitochondria in the presence of low micromolar concentrations of Ca2+ and millimolar concentrations of phosphate is known to also cause net efflux of matrix adenine nucleotides via the ATP-Mg/Pi carrier. This raises the possibility that adenine nucleotide depletion through this mechanism contributes to mitochondrial permeability transition. Results of this study show that phosphate-induced opening of the mitochondrial PTP is, at least in part, secondary to depletion of the intramitochondrial adenine nucleotide content via the ATP-Mg/Pi carrier. Delaying net adenine nucleotide efflux from mitochondria also delays the onset of phosphate-induced PTP opening. Moreover, mitochondria that are depleted of matrix adenine nucleotides via the ATP-Mg/Pi carrier show highly increased susceptibility to swelling induced by high Ca2+ concentration, atractyloside, and the prooxidant tert-butylhydroperoxide. Thus the ATPMg/Pi carrier, by regulating the matrix adenine nucleotide content, can modulate the sensitivity of rat liver mitochondria to undergo permeability transition. This has important implications for hepatocytes under cellular conditions in which the intramitochondrial adenine nucleotide pool size is depleted, such as in hypoxia or ischemia, or during reperfusion when the mitochondria are exposed to increased oxidative stress.

Effect of heat stress on muscle energy metabolism during exercise

1994 ◽  
Vol 77 (6) ◽  
pp. 2827-2831 ◽  
Author(s):  
M. A. Febbraio ◽  
R. J. Snow ◽  
C. G. Stathis ◽  
M. Hargreaves ◽  
M. F. Carey
Keyword(s):  
Heat Stress ◽  
Energy Metabolism ◽  
Relative Humidity ◽  
Energy Demand ◽  
Adenine Nucleotide ◽  
Creatine Phosphate ◽  
O2 Uptake ◽  
Muscle Energy ◽  
Muscle Energy Metabolism ◽  
Adenine Nucleotide Pool

To examine the effect of heat stress on muscle energy metabolism during submaximal exercise, 12 endurance-trained men cycled on two occasions for approximately 40 min at 70% maximal O2 uptake in an environmental chamber at either 20 degrees C and 20% relative humidity (T20) or 40 degrees C and 20% relative humidity (T40). Trials were conducted > or = 1 wk apart in random order. No difference in mean O2 uptake was observed when exercise in T40 was compared with that in T20. In contrast, exercise in T40 resulted in a higher mean heart rate (P < 0.01) and respiratory exchange ratio (P < 0.05) compared with that in T20. Postexercise rectal and muscle temperatures were also higher (P < 0.01) in T40 than in T20. Lower (P < 0.01) postexercise creatine phosphate and higher creatine (P < 0.01) and ammonia (P < 0.05) were observed in muscle after exercise in T40 compared with T20. In addition, an increased (P < 0.01) muscle glycogenolysis and higher (P < 0.01) postexercise muscle lactate accumulation were observed during exercise in T40 compared with T20. In contrast, no differences were observed in postexercise concentrations of total adenine nucleotide pool (ATP+ADP+AMP), ATP/ADP ratio, or inosine 5′-monophosphate (IMP) when T40 was compared with T20. These results indicate that the rate of ATP utilization may be increased during exercise in the heat but that this increased energy demand is predominantly met by an increase in anaerobic glycolysis and creatine phosphate hydrolysis, preventing a reduction in total adenine nucleotide pool.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of inhibiting no formation on metabolic recovery of ischemic rat heart by apelin-12

2012 ◽  
Vol 58 (6) ◽  
pp. 702-711 ◽  
Author(s):  
O.I. Pisarenko ◽  
Yu.A. Pelogeykina ◽  
V.S. Shulzhenko ◽  
I.M. Studneva ◽  
Z.D. Bespalova ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cardiac Function ◽  
Solid Phase ◽  
Adenine Nucleotide ◽  
Energy Charge ◽  
Phase Method ◽  
No Formation ◽  
Rat Hearts ◽  
Solid Phase Method ◽  
Adenine Nucleotide Pool

Apelin 12 (A-12) was synthesized by the automatic solid phase method with use of Fmoc 1H-NMR spectroscopy and mass spectrometry. Effects of apelin-12 (a peptide comprised of 12 aminoacids, A-12) on recovery of energy metabolism and cardiac function were studied in isolated working rat hearts perfused with Krebs buffer (KB) containing 11 mM glucose that were subjected to global ischemia and reperfusion. A short-term infusion of μM 140 A-12 in KB prior to ischemia enhanced myocardial ATP, the total adenine nucleotide pool (ΣAN=ATP+ADP+AMP) and the energy charge of cardiomyocites ((ATP+0.5ADP)/ΣAN) at the end of reperfusion compared with control (KB infusion) and reduced lactate content and lactate/pyruvate ratio in reperfused myocardium to the initial values. This effect was accompanied by improved recovery of coronary flow and cardiac function. Coadministration of 140 μM A-12 and 100 μM L-NAME (the nonspecific NOS inhibitor) profoundly attenuated the peptide influence on metabolic and functional recovery of reperfused hearts. The results indicate involvement of NO, formed under the peptide action, in mechanisms of cardioprotection that are tightly associated with recovery of energy metabolism in postischemic heart.

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