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Oxyfedrine and propranolol. A comparative experimental approach to protect myocardium against isoprenaline-induced myocardial necrosis.

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Myocardial necrosis was produced in rats by isoprenaline (ISP) administration (85 mg X kg-1 s.c.) for two consecutive days. Rats sacrificed at 12, 24, 30, 36 and 48 h, respectively, after the last injection of ISP showed a marked increase in serum enzymes, viz. creatine phosphokinase (CPK), lactic

Muscle phosphofructokinase deficiency (Tarui's disease): report of a case.

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A 14-year-old girl had an acute episode of rhabdomyolysis after vigorous exercise and seizures. Laboratory studies revealed elevated creatine phosphokinase (CPK) activity and myoglobinuria without acute renal failure, as well as mild indirect hyperbilirubinemia, and hyperuricemia. The elevated CPK

[Activity of the key glycolysis enzymes of the heart during emotional stress and myocardial necrosis induced after exposure to stress].

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Activities of hexokinase, phosphofructokinase and pyruvate kinase were studied in rat heart after emotional-painful stress and development of myocardium necrosis. The stress caused an activation of hexokinase and phosphofructokinase within 2 and 7 days, activity of pyruvate kinase was not altered.

[Activity of key enzymes of glycolysis in the rat liver during the development of experimental myocardial necrosis].

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Hexokinase, glucokinase, and phosphofructokinase activity in supernatant hepatic fluid obtained by centrifugation of the homogenate at 20,000 g for 20 minutes was studied during the development of experimental necrosis of the heart muscle. The activity of these enzymes was lowest in the 12th and

Effects of tumour necrosis factor-alpha on the enzymatic activities related to glucose metabolism.

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The effects of an intravenous administration of a single dose (100 micrograms/kg bw) of tumour necrosis factor-alpha (TNF, cachectin) on in vivo glucose oxidation and on several enzymatic activities related with glucose metabolism both in rat liver and skeletal muscle were studied. The treatment

Reactive oxygen species mediate the down-regulation of mitochondrial transcripts and proteins by tumour necrosis factor-alpha in L929 cells.

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In this study, we show that reactive oxygen species production induced by tumour necrosis factor alpha (TNF-alpha) in L929 cells was associated with a decrease in the steady-state mRNA levels of the mitochondrial transcript ATPase 6-8. Simultaneously, the transcript levels of two nuclear-encoded

Metabolic effects of tumour necrosis factor-alpha on rat brown adipose tissue.

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Intravenous administration of a single dose (100 micrograms/kg bw) of recombinant tumour necrosis factor-alpha (TNF, cachectin) to rats increased the rate of in vitro fatty acid synthesis in interscapular brown adipose tissue (IBAT) from both glucose and alanine, without changes in the oxidation of

Endotoxin stimulation of liver parenchymal cell phosphofructokinase activity requires nonparenchymal cells.

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The rate of carbohydrate flux through phosphofructokinase (measured as the rate of [3-3H]glucose detritiation) was increased fourfold in rat liver parenchymal cells incubated with conditioned medium from lipopolysaccharide-stimulated adherent liver non-parenchymal cells. The rate was not affected in

An extract from wax apple (Syzygium samarangense (Blume) Merrill and Perry) effects glycogenesis and glycolysis pathways in tumor necrosis factor-α-treated FL83B mouse hepatocytes.

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FL83B mouse hepatocytes were treated with tumor necrosis factor-α (TNF-α) to induce insulin resistance to investigate the effect of a wax apple aqueous extract (WAE) in insulin-resistant mouse hepatocytes. The uptake of 2-[N-(7-nitrobenz-2-oxa-1, 3-diazol-4-yl)amino]-2-deoxyglucose (2 NBDG), a

Fructose-1,6-Bisphosphate Protects Hippocampal Rat Slices from NMDA Excitotoxicity.

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Effects of fructose 1,6-bisphosphate (F-1,6-P2) towards N-methyl-d-aspartate NMDA excitotoxicity were evaluated in rat organotypic hippocampal brain slice cultures (OHSC) challenged for 3 h with 30 μM NMDA, followed by incubations (24, 48, and 72 h) without (controls) and with F-1,6-P2 (0.5,

Glycolytic and immunological alterations in human U937 monocytes in response to H1N1 infection

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We monitored changes that took place in glycolytic enzymes, the pyruvate end product of glycolysis, tumor necrosis factor α (TNFα), and toll-like receptors (TLRs) both at the transcriptional and translational levels upon direct interaction between PR8-H1N1 and the human monocytes U937 in vitro

Thermogenic protein UCP1 and UCP3 expression in non-small cell lung cancer: relation with glycolysis and anaerobic metabolism.

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Uncoupling protein 1 (UCP1) is a proton transporter/channel residing on the inner mitochondrial membrane and is involved in cellular heat production. Using immunohistochemistry, we investigated the expression of UCP1 and UCP3 in a series of 98 patients with non-small cell lung cancer (NSCLC) treated

Bone morphogenetic protein 15 and fibroblast growth factor 10 enhance cumulus expansion, glucose uptake, and expression of genes in the ovulatory cascade during in vitro maturation of bovine cumulus-oocyte complexes.

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Oocyte-secreted factors (OSFs) regulate differentiation of cumulus cells and are of pivotal relevance for fertility. Bone morphogenetic protein 15 (BMP15) and fibroblast growth factor 10 (FGF10) are OSFs and enhance oocyte competence by unknown mechanisms. We tested the hypothesis that BMP15 and

Antagonistic effects of selenium on cadmium-induced apoptosis by restoring the mitochondrial dynamic equilibrium and energy metabolism in chicken spleens.

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The aim of this study was to investigate the mechanism of cadmium-induced apoptosis in chicken spleens and the antagonistic effects of selenium. We duplicated the selenium-cadmium interaction model and examined the expression of apoptosis-, immune-, mitochondrial dynamics- and energy

Biochemical and histopathological alterations in golden hamster during infection with Ancylostoma ceylanicum.

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Ancylostoma ceylanicum infection in golden hamsters (Mesocricetus auratus) caused marked biochemical and histopathological derangements. Jejunum, the primary site of infection, showed pronounced alterations compared with liver. Though the biochemical composition of jejunum was not significantly

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