scholarly journals Amelioration of Energy Metabolism by Melatonin in Skeletal Muscle of Rats With LPS Induced Endotoxemia

2016 ◽  
pp. 833-842 ◽  
Author(s):  
E. OZKOK ◽  
H. YORULMAZ ◽  
G. ATES ◽  
A. AKSU ◽  
N. BALKIS ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Muscle Tissue ◽  
High Performance ◽  
Succinic Dehydrogenase ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
Creatine Phosphate ◽  
Before And After ◽  
Hematoxylin And Eosin

In the literature, few studies have investigated the effects of melatonin on energy metabolism in skeletal muscle in endotoxemia. We investigated the effects of melatonin on tissue structure, energy metabolism in skeletal muscle, and antioxidant level of rats with endotoxemia. We divided rats into 4 groups, control, lipopolysaccharide (LPS) (20 mg/kg, i.p., single dose), melatonin (10 mg/kg, i.p., three times), and melatonin + LPS. Melatonin was injected i.p. 30 min before and after the 2nd and 4th hours of LPS injection. Antioxidant status was determined by glutathione (GSH) measurement in the blood. Muscle tissue was stained using modified Gomori trichrome (MGT), succinic dehydrogenase (SDH), and cytochrome oxidase (COX) and histological scored. Also the sections were then stained with hematoxylin and eosin. The stained sections were visualized and photographed. Creatine, creatine phosphate, adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) levels were investigated using high performance liquid chromatography (HPLC) in muscle tissue. In the Melatonin + LPS group, blood GSH levels were increased compared with the LPS group (P<0.01). Melatonin reduced myopathic changes in the LPS group according to the histopathologic findings. In addition, ATP values were increased compared with the LPS group (P<0.05). Our findings showed melatonin treatment prevented muscle damage by increasing ATP and GSH levels in rats with LPS induced endotoxemia.

scholarly journals Zinc-induced platelet aggregation is mediated by the fibrinogen receptor and is not accompanied by release or by thromboxane synthesis

Blood ◽  
1985 ◽  
Vol 66 (1) ◽  
pp. 213-219 ◽  
Author(s):  
P Heyns A du ◽  
A Eldor ◽  
R Yarom ◽  
G Marx
Keyword(s):  
Platelet Aggregation ◽  
Dense Body ◽  
Platelet Rich Plasma ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
Creatine Phosphate ◽  
Calcium Flux ◽  
Fibrinogen Receptor ◽  
Induced Aggregation

Abstract We demonstrate that zinc (0.1 to 0.3 mmol/L) induces aggregation of washed platelet suspensions. Higher concentrations (1 to 3 mmol/L) of zinc were needed to aggregate platelets in platelet-rich plasma obtained from blood anticoagulated with low-molecular-weight heparin, probably due to the binding of zinc to the plasma proteins. Zinc- induced aggregation of normal washed platelets required added fibrinogen and no aggregation occurred with thrombasthenic platelets or with normal platelets pretreated with a monoclonal antibody (10E5) that blocks the platelet fibrinogen receptor. These data indicate that the platelet membrane fibrinogen receptor-glycoproteins IIb and IIIa mediate the effect of zinc. Zinc-induced aggregation was blocked by the agent TMB-8, which interferes with the internal calcium flux, and by prostacyclin, which elevates platelet cyclic adenosine monophosphate levels. Zinc-induced aggregation was not accompanied by thromboxane synthesis or by the secretion of dense-body serotonin and was not affected by preexposure of platelets to acetylsalicylic acid. Experiments with creatine phosphate/creatine phosphokinase showed that the zinc effect on platelets was independent of extracellular adenosine diphosphate (ADP). Zinc had an additive effect when platelet aggregation was stimulated with subthreshhold concentrations of collagen or ADP. Together with the known effects of nutritional zinc on in vivo bleeding, on platelet aggregation, and on lipid metabolism, the results suggest that zinc may have an important bearing on normal hemostasis, thrombosis, and atherosclerosis.

Content Variations of ATP-Related Compounds and Quality Assessment of Tilapia Fillets during Iced Storage

2014 ◽  
Vol 1073-1076 ◽  
pp. 1767-1775
Author(s):  
Lei Lei Sun ◽  
Hui Huang ◽  
Lai Hao Li ◽  
Xian Qing Yang ◽  
Shu Xian Hao ◽  
...  
Keyword(s):  
Quality Assessment ◽  
High Performance ◽  
Storage Time ◽  
Degradation Products ◽  
Thiobarbituric Acid ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
Significant Linear Correlation ◽  
Tilapia Fillets ◽  
Iced Storage

To explore the biochemical changes of tilapia fillets during iced storage, contents of adenosine triphosphate (ATP) and its degradation products were monitored by high performance liquid chromatography (HPLC), along with ATPase and the freshness indicators such as the values ofK,Ki,H,Fr, total volatile base nitrogen (TVB-N) and thiobarbituric acid (TBA) were determined to evaluate the quality of iced tilapia fillets. The results showed that ATP, adenosine diphosphate (ADP) and adenosine monophosphate (AMP) in iced tilapia fillets degraded sharply into inosine monophosphate (IMP) at the first day of storage, then almost kept stable in a low level over the rest of iced storage time. Meanwhile, IMP degraded into hypoxantjine (Hx) and inosine (HxR) with the extending storage time, and Hx as well as HxR accumulated. The changes of values ofK,Ki,H,Frwith iced storage time presented a significant linear correlation (P<0.01, r=0.945, 0.943, 0.924, -0.943, respectively). ATPase activities were associated with the degradation of ATP. The contents of IMP, Hx, HxR, values ofK,Ki,H,Frand ATPase activities can be used as practical and effective indicators for quality assessment of tilapia fillets during iced storage instead of TVB-N and TBA.

THE INFLUENCE OF SYMPATHOMIMETIC AMINES, MONOAMINE OXIDASE INHIBITORS, AND ANTIHYPERTENSIVES UPON THE ENERGY METABOLISM IN THE RAT HEART

1966 ◽  
Vol 44 (4) ◽  
pp. 605-613 ◽  
Author(s):  
W. G. Hilliard ◽  
W. T. Oliver ◽  
G. R. Van Petten
Keyword(s):  
Energy Metabolism ◽  
Monoamine Oxidase ◽  
Rat Heart ◽  
Antihypertensive Drugs ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
Monoamine Oxidase Inhibitors ◽  
Sympathomimetic Amines ◽  
Cardiac Energy Metabolism

This investigation was undertaken to determine the effects of three classes of catecholamine-releasing drugs on cardiac energy metabolism. The levels of adenosine monophosphate (AMP), adenosine diphosphate (ADP), adenosine triphosphate (ATP), inorganic phosphate (IP), and phosphocreatine (CP) of the rat heart were measured. The sympathomimetic amines tyramine, ephedrine, methylamphetamine, and (+)- and (−)-amphetamine caused significant decreases in CP. Tyramine and (+)- and (−)-amphetamine also significantly depressed ATP. Of the antihypertensive drugs investigated, bretylium and guanethidine decreased the amount of CP present, and the latter compound also significantly decreased ATP. The administration of reserpine was without significant effect on cardiac high-energy phosphate levels. Among the monoamine oxidase inhibitors, tranylcypromine significantly lowered ATP and CP, whereas pheniprazine produced no significant changes. This study showed that those drugs which have been reported to release cardiac catecholamines also reduced cardiac levels of CP and ATP. The hypothesis is advanced that this effect is due to increased utilization of energy by two mechanisms: (a) stimulation of the active recapture mechanism for adrenergic neurotransmitters, and (b) the positive inotropic and chronotropic responses of the heart to the drug-released catecholamines. In either case, the observed decreases in the levels of ATP and CP in the heart are effects of sympathomimetic amines which have been heretofore unreported.

Skeletal muscle physiology and damage

2018 ◽  
Author(s):  
Robert Dinser ◽  
Ulf Müller-Ladner
Keyword(s):  
Molecular Structure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Muscle Tissue ◽  
Muscle Function ◽  
Clinical Analysis ◽  
Basic Function ◽  
Muscle Disease ◽  
Muscle Physiology ◽  
Physiological Ageing

This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.

DEGRADATION OF ADENINE NUCLEOTIDES IN THE MUSCLE OF THE DUNGENESS CRAB (CANCER MAGISTER) AND KING CRAB (PARALITHODES CAMTSCHATICA) DURING STORAGE AND COOKING

1969 ◽  
Vol 32 (1) ◽  
pp. 1-3 ◽  
Author(s):  
H. S. Groninger ◽  
K. R. Brandt
Keyword(s):  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
Heat Processing ◽  
Minor Role ◽  
Dungeness Crab ◽  
Cancer Magister ◽  
King Crab ◽  
Before And After

The adenine nucleotide content of king and Dungeness crab was determined on muscle before and after storage and on heat-processed or cooked crab meat. As a result of both storage and heat processing, adenosine triphosphate (ATP) and adenosine diphosphate (ADP) are degraded to adenosine monophosphate (AMP) and inosine and hypoxanthine. Only small amounts of inosine monophosphate (IMP) are found in cooked crabmeat. Flavor evaluation of IMP-treated king crab showed that IMP plays only a minor role in the flavor of crab.

Temporal profile and significance of metabolic failure and trophic changes in the canine cerebral arteries during chronic vasospasm after subarachnoid hemorrhage

1993 ◽  
Vol 78 (5) ◽  
pp. 807-812 ◽  
Author(s):  
Yuhei Yoshimoto ◽  
Phyo Kim ◽  
Tomio Sasaki ◽  
Kintomo Takakura
Keyword(s):  
Subarachnoid Hemorrhage ◽  
High Performance ◽  
Close Association ◽  
Cerebral Arteries ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphates ◽  
Content Type ◽  
Temporal Profile

✓ To investigate the pathogenetic significance of metabolic failure observed in spastic cerebral arteries after subarachnoid hemorrhage (SAH), the temporal profile of alterations in the arterial content of high-energy phosphates was studied. A canine model of double hemorrhage was used. Constriction of the basilar artery was measured angiographically on Days 3, 5, 7, and 14 after SAH in separate groups of animals. Adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), guanosine triphosphate (GTP), guanosine diphosphate, creatine phosphate (CrP), and creatine (Cr) levels in the arteries were assayed using high-performance liquid chromatography. A time-dependent development of angiographic spasm was confirmed. A mild vasospasm was seen in the group studied 3 days after SAH, progressed in the Day 5 group, remained comparably severe in the Day 7 group, and resolved partially in the Day 14 group. The content of high-energy phosphates (ATP, GTP, and CrP) declined rapidly over the course of the study, and a significant reduction in ATP, GTP, and CrP was observed in the Day 3 group. Levels of ATP and CrP decreased further in the Day 5 and 7 groups. The decrement in GTP was completed in the early phase; a significant reduction took place in the Day 3 group, with no progression thereafter and no recovery though Day 14. Total adenylate (ATP + ADP + AMP) and total creatine (Cr + CrP) content diminished markedly over the course of the study. These results indicate that metabolic failure and trophic disturbance in the cerebral artery occurs with a rapid onset following SAH and progresses in close association with the development of vasospasm, suggesting a significant causal relationship with the pathogenesis.

Skeletal muscle physiology and damage

2013 ◽  
pp. 404-408
Author(s):  
Robert Dinser ◽  
Ulf Müller-Ladner
Keyword(s):  
Molecular Structure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Muscle Tissue ◽  
Muscle Function ◽  
Clinical Analysis ◽  
Basic Function ◽  
Muscle Disease ◽  
Muscle Physiology ◽  
Physiological Ageing

This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.

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