cytochrome oxidase/inflammation

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Nitric oxide inhibition of cytochrome oxidase and mitochondrial respiration: implications for inflammatory, neurodegenerative and ischaemic pathologies.

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Nitric oxide (NO) at high levels is cytotoxic, and may be involved in a range of inflammatory, neurodegenerative, and cardiovascular/ischaemic pathologies. The mechanism of NO-induced cytotoxicity is unclear. Recently we and others have found that low (nanomolar) levels of NO reversibly inhibit

Inflammatory myopathy with cytochrome oxidase negative muscle fibers: methotrexate treatment.

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Inflammatory myopathy with cytochrome oxidase negative muscle fibers (IM/COX-) is characterized by slowly progressive weakness, most prominent in the quadriceps, muscle fibers with reduced COX staining and mitochondrial DNA mutations, and a poor response to corticosteroid treatment. We reviewed

[General activity and isoenzyme spectrum of cytochrome oxidase and malate dehydrogenase in acute and chronic pneumonia with different degrees of inflammation].

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[On succinic dehydrogenase and cytochrome oxidase in chronic inflammation of the nasal mucous membrane].

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The activity of cytochrome oxidase is increased in circulating lymphocytes of patients with chronic obstructive pulmonary disease, asthma, and chronic arthritis.

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We have previously shown that the activity of cytochrome oxidase (CytOx) in skeletal muscle of patients with chronic obstructive pulmonary disease (COPD) was higher than in healthy control subjects. The mechanisms and implications of this observation were unclear. In particular, it was not known if

Oxaloacetate activates brain mitochondrial biogenesis, enhances the insulin pathway, reduces inflammation and stimulates neurogenesis.

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Brain bioenergetic function declines in some neurodegenerative diseases, this may influence other pathologies and administering bioenergetic intermediates could have therapeutic value. To test how one intermediate, oxaloacetate (OAA) affects brain bioenergetics, insulin signaling, inflammation and

Paeonol increases levels of cortical cytochrome oxidase and vascular actin and improves behavior in a rat model of Alzheimer's disease.

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Paeonol(2'-hydroxy-4'-methoxyacetophenone;1-(2-hydroxy-4-methoxyphenyl)ethan-1-one) is a constituent of the bark of the Moutan Cortex (Paeonia suffruticosa). This bark has been used as a traditional Chinese medicine and is reputed to possess a broad range of therapeutic properties probably by virtue

Inflammatory myopathies with mitochondrial pathology and protein aggregates.

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OBJECTIVE To compare the clinical course and muscle biopsy features of polymyositis with mitochondrial pathology (PM-Mito) to inclusion body myositis (IBM) and steroid-responsive inflammatory myopathies (polymyositis). METHODS We compared clinical, laboratory and myopathologic features in a

Down-regulation of miR-301a suppresses pro-inflammatory cytokines in Toll-like receptor-triggered macrophages.

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In many types of tumours, especially pancreatic adenocarcinoma, miR-301a is over-expressed. This over-expression results in negative regulation of the target gene of miR-301a, the nuclear factor-κB (NF-κB) repressing factor (NKRF), increasing the activation of NF-κB and production of

Increased cytochrome oxidase activity in alkali-burned corneas.

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Cytochrome oxidase (CO) activity on alkali-burned rabbit corneas was investigated histochemically to determine the metabolic change in inflamed corneas during wound healing. Cryostat sections of chemically burned and mechanically scraped corneas were stained for CO activity, which is regarded as an

Rat models of dementia based on reductions in regional glucose metabolism, cerebral blood flow and cytochrome oxidase activity.

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Three models are described in rats which attempt to mimic morphological and behavioural pathology of Alzheimer's dementia; intracerebroventricular injection of streptozotocin (STZ), permanent bilateral carotid artery occlusion (2VO) and brain mitochondrial cytochrome oxidase inhibition by sodium

N-Adamantyl-4-Methylthiazol-2-Amine Attenuates Glutamate-Induced Oxidative Stress and Inflammation in the Brain.

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In this study, we explored the possible mechanisms underlying the neuroprotective and anti-oxidative effects of N-adamantyl-4-methylthiazol-2-amine (KHG26693) against in vivo glutamate-induced toxicity in the rat cerebral cortex. Our results showed that pretreatment with KHG26693 significantly

Nitric oxide, hypoxia and brain inflammation.

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NO (nitric oxide) acutely and potently inhibits mitochondrial cytochrome oxidase in competition with oxygen, thereby raising the apparent K(M) for oxygen of mitochondria and neurons into the physiological or pathological range. We find that NO from an NO donor or glial inducible NOS (nitric oxide

Reversible inhibition of cellular respiration by nitric oxide in vascular inflammation.

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Incubation of rat aortas with endotoxin and interferon-gamma for 24 h resulted in an aortic oxygen consumption that was substantially inhibited and strongly oxygen dependent (37% inhibition at 160 microM O(2) and 62% inhibition at 80 microM O(2) relative to untreated aortas). This respiratory

Metabolic impairment induces oxidative stress, compromises inflammatory responses, and inactivates a key mitochondrial enzyme in microglia.

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Microglial activation, oxidative stress, and dysfunctions in mitochondria, including the reduction of cytochrome oxidase activity, have been implicated in neurodegeneration. The current experiments tested the effects of reducing cytochrome oxidase activity on the ability of microglia to respond to

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