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Increase of cytochrome c oxidase negative fibers in rimmed vacuole myopathy with inflammatory changes.

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The physiological significance of cytochrome c oxidase (CCO) deficiency in rimmed vacuole myopathy (RVM) is not fully understood. Frequencies of CCO negative muscle fibers (CCO(-)F) were compared with two cases of in-clusion body myositis (IBM) and another two cases with RVM without inflammatory

Cytochrome c oxidase deficiencies in the muscle of patients with inflammatory myopathies.

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We studied mitochondrial function in inflammatory myopathies, using cytochrome c oxidase (COX) reaction on muscle biopsy samples from 30 patients (15 with dermatomyositis, 12 with polymyositis, and 3 with inclusion body myositis) and 30 age-matched controls. We also performed immunocytochemistry for

Effect of dextran sulfate sodium and acute exercise on mouse intestinal inflammation and lymphocyte cytochrome c levels.

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OBJECTIVE Athletes may experience gastrointestinal disturbances during intense exercise. Using a mouse model, we determined the influence of acute exercise (AE) and dextran sulfate sodium (DSS), a chemical known to induce intestinal inflammation, on: 1) inflammatory changes within small and large

Serum cytochrome c level as a prognostic indicator in patients with systemic inflammatory response syndrome.

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BACKGROUND Apoptosis may play an important role in the development of systemic inflammatory response syndrome (SIRS) and progression to multiple organ dysfunction syndrome (MODS). To quantify the extent of apoptosis in these morbidities, we developed a sandwich ELISA system to measure serum

SMAC mimetics sensitize nonsteroidal anti-inflammatory drug-induced apoptosis by promoting caspase-3-mediated cytochrome c release.

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Nonsteroidal anti-inflammatory drugs (NSAID) are effective in suppressing the formation of colorectal tumors. However, the mechanisms underlying the antineoplastic effects of NSAIDs remain unclear. The effects of NSAIDs are incomplete, and resistance to NSAIDs is often developed. Growing evidence

Regulation of mitochondrial respiration and apoptosis through cell signaling: cytochrome c oxidase and cytochrome c in ischemia/reperfusion injury and inflammation.

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Cytochrome c (Cytc) and cytochrome c oxidase (COX) catalyze the terminal reaction of the mitochondrial electron transport chain (ETC), the reduction of oxygen to water. This irreversible step is highly regulated, as indicated by the presence of tissue-specific and developmentally expressed isoforms,

Treatment with 670 nm light up regulates cytochrome C oxidase expression and reduces inflammation in an age-related macular degeneration model.

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Inflammation is an umbrella feature of ageing. It is present in the aged retina and many retinal diseases including age-related macular degeneration (AMD). In ageing and in AMD mitochondrial function declines. In normal ageing this can be manipulated by brief exposure to 670 nm light on the retina,

Promotion of oxidative damage to arachidonic acid and alpha 1-antiproteinase by anti-inflammatory drugs in the presence of the haem proteins myoglobin and cytochrome C.

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A mixture of myoglobin and hydrogen peroxide (H2O2) causes peroxidation of arachidonic acid. This peroxidation is greatly accelerated by adding phenylbutazone, which is effective even in the absence of H2O2. A wide range of other drugs was examined for their ability to exert similar pro-oxidant

Camel whey protein enhances lymphocyte survival by modulating the expression of survivin, bim/bax, and cytochrome C and restores heat stress-mediated pathological alteration in lymphoid organs.

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Heat stress (HS) is a catastrophic stressor that dampens immunity. The current study investigates the effect of dietary administration with camel whey protein (CWP) on apoptotic pathway caused by HS.Forty-five male mice were divided into three groups: a

Genetic and histologic evidence implicates role of inflammation in traumatic brain injury-induced apoptosis in the rat cerebral cortex following moderate fluid percussion injury.

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Traumatic brain injury (TBI) causes massive brain damage. However, the secondary injury and temporal sequence of events with multiple mechanisms after the insult has not been elucidated. Here, we examined the occurrence of apoptosis and a causal relationship between inflammation and apoptosis in the

Cardiac mitochondrial damage and inflammation responses in sepsis.

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OBJECTIVE Studies in sepsis suggest that mitochondria mediate multiple organ dysfunction, including cardiac failure; however, the underlying molecular mechanisms remain elusive. This study examined changes in mitochondrial membrane integrity, antioxidant activities, and oxidative stress in the heart

Alanyl-glutamine improves pancreatic β-cell function following ex vivo inflammatory challenge.

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Obesity-associated diabetes and concomitant inflammation may compromise pancreatic β-cell integrity and function. l-glutamine and l-alanine are potent insulin secretagogues, with antioxidant and cytoprotective properties. Herein, we studied whether the dipeptide l-alanyl-l-glutamine (Ala-Gln) could

Mesalazine Induces Oxidative Stress and Cytochrome c Release in Isolated Rat Heart Mitochondria: An Analysis of Cardiotoxic Effects.

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Mesalazine is widely used in the management of inflammatory bowel disease. Previous studies reported that mesalazine-induced cardiotoxicity is a rare, potentially fatal complication. Mitochondria play an important role in myocardial tissue homeostasis. Deterioration in mitochondrial function will

Antioxidant, anti-inflammatory and hepatoprotective effects of silymarin on hepatic dysfunction induced by sodium nitrite.

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OBJECTIVE Sodium nitrite, a food additive that is used as a color fixative and preservative for meats and fish, has been reported to have adverse health effects due to increased oxidative stress that could be harmful to different organs including the liver. Meanwhile, silymarin protects against

Solasonine inhibits glioma growth through anti-inflammatory pathways.

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The global burden of malignant glioma is expected to increase and new therapy approaches are urgently required. Solasonine is a natural glycoalkaloid compound that has been used in cancer treatment for many years; however the precise mechanisms are poorly understood. Here we seek to explore the

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