adenosine triphosphate/nekrose

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Exogenous magnesium chloride-adenosine triphosphate administration during reperfusion reduces the extent of necrosis in previously ischemic skeletal muscle.

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The lower extremity may be exposed to prolonged periods of ischemia, resulting in depletion of intracellular energy stores in the affected skeletal muscle. The role of adenine nucleotide reduction and failure of resynthesis on reperfusion in determining the extent of muscle necrosis was investigated

Adenosine triphosphate hydrolysis reduces neutrophil infiltration and necrosis in partial-thickness scald burns in mice.

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Extracellular adenosine triphosphate (ATP), present in thermally injured tissue, modulates the inflammatory response and causes significant tissue damage. The authors hypothesize that neutrophil infiltration and ensuing tissue necrosis would be mitigated by removing ATP-dependent signaling at the

Intracellular adenosine triphosphate (ATP) concentration: a switch in the decision between apoptosis and necrosis.

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Apoptosis and necrosis are considered conceptually and morphologically distinct forms of cell death. Here, we report that demise of human T cells caused by two classic apoptotic triggers (staurosporin and CD95 stimulation) changed from apoptosis to necrosis, when cells were preemptied of adenosine

Mitochondrial proteins that regulate apoptosis and necrosis are induced in mouse fatty liver.

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Fatty liver is common in nonalcoholic, obese individuals and in lean people who consume alcohol chronically. Although fatty liver is typically benign, a subset of individuals with steatosis develop steatohepatitis and eventually cirrhosis. The disparate outcomes of fatty liver suggest that it

Regulation of the apoptosis-necrosis switch.

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Execution of the apoptotic program involves a relatively limited number of pathways. According to a general view, these would converge to activate the caspase family of proteases. However, there is increasing evidence that apoptotic-like features can also be found when caspases are inhibited.

Glycine preserves function and decreases necrosis in skeletal muscle undergoing ischemia and reperfusion injury.

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BACKGROUND Glycine (GLY) is a neutral amino acid that has been shown to be cytoprotective in the kidneys of dogs and rabbits undergoing ischemia-reperfusion injury. To investigate whether GLY exhibits a protective effect on skeletal muscle subjected to ischemia and reperfusion injury, we used a

Efficacy of Shoushen granule on adenosine triphosphate binding cassette transporter A1, proprotein convertase subtilisin/kexin type 9 and toll-like receptor 4/nuclear factor kappa-B signaling pathway in ApoE-knockout mice.

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To evaluate the efficacy of Shoushen granule, prepared with four Chinese medicinals, on the targeted regulation of adenosine triphosphate binding cassette transporter A1 (ABCA1) through proprotein convertase subtilisin/kexin type 9 (PCSK9) and toll-like receptor 4 (TLR4) / nuclear

Anandamide induces necrosis in primary hepatic stellate cells.

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The endogenous cannabinoid anandamide (AEA) is a lipid mediator that blocks proliferation and induces apoptosis in many cell types. Although AEA levels are elevated in liver fibrosis, its role in fibrogenesis remains unclear. This study investigated effects of AEA in primary hepatic stellate cells

Nitric oxide induces apoptosis via hydrogen peroxide, but necrosis via energy and thiol depletion.

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We investigated the mechanisms by which two nitric oxide (NO) donors, diethylenetriamine/NO adduct (DETA/NO) and S-nitrosoglutathione (GSNO), induced cell death in a J774 macrophage cell line. Both NO donors induced caspase activation within 6 h, but only DETA/NO-induced caspase activation was

Phosphoenolpyruvate/adenosine triphosphate enhances post-ischemic survival of skeletal muscle.

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This study examined whether ischemia-reperfusion injury to skeletal muscle could be reduced by post-ischemic infusion of phosphoenolpyruvate (PEP) and adenosine triphosphate (ATP). The rectus femoris muscle of 54 rabbits was rendered ischemic for 3.5 hr. Eighteen rabbits received no further

Improved ischemic island skin flap survival with continuous intraarterial infusion of adenosine triphosphate--magnesium chloride and superoxide dismutase: a rat model.

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Neurovascular island skin flaps are still hampered by occasional necrosis of their most distal aspect. Cells subjected to prolonged hypoxic conditions become intracellularly depleted of needed metabolic substrates and eventually die. Once hypoxic conditions are improved, ischemic tissue suffers

Calcium and adenosine triphosphate control of cellular pathology: asparaginase-induced pancreatitis elicited via protease-activated receptor 2.

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Exocytotic secretion of digestive enzymes from pancreatic acinar cells is elicited by physiological cytosolic Ca(2+) signals, occurring as repetitive short-lasting spikes largely confined to the secretory granule region, that stimulate mitochondrial adenosine triphosphate (ATP) production. By

Alterations in the indexes of apoptosis and necrosis induced by galactosamine in the liver of Wistar rats treated with fructose-1,6-bisphosphate.

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Galactosamine (GalN) is a hepatotoxic agent, which under determined situations provokes metabolic and energetic depletion as well as alterations in permeability, leading to cellular death. At the same time, it is known that fructose-1,6-bisphosphate (FBP) helps maintain cell energy levels and

Impaired autophagic clearance after cold preservation of fatty livers correlates with tissue necrosis upon reperfusion and is reversed by hypothermic reconditioning.

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Fatty livers are particularly susceptible to mitochondrial alterations after cold preservation. We thus aimed to improve graft integrity by brief hypothermic oxygenation prior to warm reperfusion. Macrovesicular steatosis was induced in rat livers by fasting and subsequent feeding of a fat-free diet

Induced hypothermia is protective in a rat model of pneumococcal pneumonia associated with increased adenosine triphosphate availability and turnover*.

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OBJECTIVE To determine the effect of induced hypothermia on bacterial growth, lung injury, and mitochondrial function in a rat model of pneumococcal pneumosepsis. METHODS Animal study. METHODS University research laboratory. METHODS Male Sprague-Dawley rats. METHODS Subjects were inoculated

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