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Ground bovine longissimus and rabbit white muscles were frozen (-25 degrees C) in the prerigor state and subsequently thawed(+20 degrees C) to determine the combined effect of grinding and freezing on glycolytic metabolites and enzymes. Frozen ground muscle, when compared to unfrozen ground tissue, showed significantly lower hexose monophosphates and significantly greater levels of all metabolites from fructose diphosphate to phosphoenolpyruvate, indicating activation of phosphofructokinase and inhibition of pyruvate kinase during the freezing process. Thawing caused rapid glycolysis and the metabolites returned to near unfrozen levels by the time glycolysis ceased, due to strong activation of phosphorylase by Ca2+. Both muscle types had a similar pattern of changes.
The effects of the sulfydryl donor drug N-(2-mercaptopropionyl)-glycine (MPG) on neutrophil chemotaxis, adhesiveness, phagocytosis, and hexose monophosphate shunt activity were investigated in vitro. The drug significantly enhanced all the neutrophil functions tested when used at appropriate concentrations. The results, which are in accord with the well known inhibition of neutrophil function by sulfydryl-blocking agents, suggest the possible therapeutic usefulness of the drug in clinical conditions with defective neutrophil function.
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Long-term exposure of rats to isoproterenol and dopamine resulted in an increase of glucose-6-phosphate dehydrogenase activity and a greater availability of 5-phosphoribosyl-l-pyrophosphate in the myocardium. These results are interpreted to indicate an enhanced flow through the hexose monophosphate shunt.
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Benoxaprofen inhibited the random motility and migration to the leucoattractants endotoxin-activated serum (EAS) and f-met-leu-phe of human polymorphonuclear leucocytes (PMNL) in vitro. Inhibition of random and leucoattractant-induced migration was observed at drug concentrations of greater than 1 X 10(-6) M and 1 X 10(-5) M respectively. Benoxaprofen per se was not leucotactic but was pro-oxidative in that it stimulated PMNL hexose-monophosphate shunt activity, chemiluminescence, myeloperoxidase-mediated iodination reactions and degranulation. The drug also mediated auto-oxidation of PMNL as measured by cellular auto-iodination. The relationship between benoxaprofen-mediated inhibition of PMNL migration and activation of oxidative metabolism was investigated using the anti-oxidants ascorbate and levamisole at concentrations of 10(-2) M and 10(-3) M respectively. These agents prevented the decreased motility and auto-oxidation of PMNL induced by 10(-4) M benoxaprofen. Benoxaprofen (10(-4) M) did not inhibit the migration of PMNL from 3 children with chronic granulomatous disease thus showing that intact PMNL oxidative metabolism is required for the induction of drug-mediated inhibition of cell motility. Ingestion of therapeutic doses of benoxaprofen for 7 days by normal adults gave serum drug concentrations greater than those required for detectable effects on PMNL functions in vitro (mean serum value 126 micrograms/ml). Co-incubation of normal PMNL with serum from individuals who had ingested the drug caused decreased cell migration and increased chemiluminescence. These results show that benoxaprofen inhibits PMNL migration as a consequence of pro-oxidant properties and despite its withdrawal may be the prototype of the pro-oxidative anti-inflammatory drug.
1. In three models of cardiac hypertrophy in rats (aortic constriction, application of a single dose of isoproterenol and daily injections of triiodothyronine) the biosynthesis of myocardial adenine nucleotides was enhanced. 2. In hypertrophying hearts due to aortic constriction and isoproterenol application, the activity of glucose-6-phosphate dehydrogenase and the available pool of 5-phosphoribosyl-1-pyrophosphate were increased indicating a stimulation of the hexose monophosphate shunt. In triiodothyronine-treated animals only the cardiac pool of 5-phosphoribosyl-1-pyrophosphate turned out to be elevated. 3. In all three models of cardiac hypertrophy, the enhancement of myocardial adenine nucleotide biosynthesis was exaggerated by ribose. It thus appears that the 5-phosphoribosyl-1-pyrophosphate pool is the limiting factor for the increase of adenine nucleotide biosynthesis under these conditions. 4. Long-term i.v. infusion of ribose (200 mg/kg/h) in isoproterenol-treated rats prevented the decrease of the cardiac ATP concentration induced by isoproterenol. However, the isoproterenol-induced stimulation of total cardiac protein synthesis was not altered, suggesting that the ATP decline may not be the trigger for stimulating protein synthesis in this model of myocardial hypertrophy.
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Apatite formation from synthetic extracellular fluids is rate-limited both at the initial amorphous precursor deposition step and at the amorphous-crystalline transformation reaction. Nucleotide diphosphates and triphosphates and low molecular weight metabolites containing two attached ester phosphate groups all inhibited amorphous-crystalline conversion at concentrations of 10(-5) to 10(-6)M. Both native and synthetic polynucleotides as well as the phosphoproteins from rat dentin or egg yolk also inhibited crystal formation from amorphous calcium phosphate. In all cases, substantial amounts of inhibitor molecules were incorporated into the stabilized amorphous precipitates. Treatment of isolated, inhibitor-stabilized amorphous precipitates with hydrolytic enzymes such as alkaline phosphatase or papain reversed the inhibitory effect and permitted crystallization to proceed normally.