cytochrome oxidase/nekróza

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p53 and tumor necrosis factor alpha regulate the expression of a mitochondrial chloride channel protein.

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A novel chloride intracellular channel (CLIC) gene, clone mc3s5/mtCLIC, has been identified from differential display analysis of differentiating mouse keratinocytes from p53+/+ and p53-/- mice. The 4.2-kilobase pair cDNA contains an open reading frame of 762 base pairs encoding a 253-amino acid

Olfactory mucosal necrosis in male CD rats following acute inhalation exposure to hydrogen sulfide: reversibility and the possible role of regional metabolism.

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Hydrogen sulfide (H2S) is a potent inhibitor of cytochrome oxidase (CO) and is associated with dysosmia and anosmia in humans and nasal lesions in exposed rodents. An improved understanding of the pathogenesis of these lesions is needed to determine their toxicological relevance. We exposed

Inhibition of tumour necrosis factor-alpha (TNFalpha)-induced NF-kappaB p52 converts the metabolic effects of microglial-derived TNFalpha on mouse cerebellar neurones to neurotoxicity.

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Activated microglia are implicated in the injury of neurones and macroglia both in vitro and in vivo. Here, we demonstrate that media conditioned by interferon-gamma treated microglia initially impair the metabolism of mouse cerebellar neurones grown in serum-free conditions without inducing cell

Caspase-3-associated apoptotic cell death in excitotoxic necrosis of the entorhinal cortex following intraperitoneal injection of kainic acid in the rat.

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The present study is directed to study: (a) bax translocation and cytochrome c release as mediators of the mitochondrial pathway of apoptosis; (b) Fas-L (Fas-ligand) expression as an indicator of the possible involvement of the Fas/Fas-L signaling pathway; and (c) active caspase-3 expression as the

Inhibition of target cell mitochondrial electron transfer by tumor necrosis factor.

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Using digitonin permeabilization to assay mitochondrial electron transfer, we have found that respiratory activity (succinoxidase and cytochrome oxidase) in three mouse fibroblast lines is completely eliminated by incubation with human recombinant tumor necrosis factor-alpha (hrTNF). As with

Acid hydrolase and cytochrome oxidase activities in nitrosourea induced tumors of the nervous system.

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Nitrosourea induced tumors of the nervous system in rats have proven useful for biochemical studies combined with morphological approaches. The pattern of enzyme activities for acid hydrolases and cytochrome oxidase resemble those previously observed in spontaneous nervous system tumors of man. The

Tumor necrosis factor-alpha plus actinomycin D-induced apoptosis of L929 cells is prevented by nitric oxide.

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Treatment with the nitric oxide-(NO)-generating compound S-nitroso-N-acetylpenicillamine protected cul-tured L929 cells from apoptosis induced by tumor necrosis factor-alpha (TNF-alpha) plus actinomycin D, as determined by the detection of DNA fragmentation and morphological changes. NO also

2,3,6-triaminopyridine, a metabolite of the urinary tract analgesic phenazopyridine, causes muscle necrosis and renal damage in rats.

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Some aromatic polyamines form very stable free radicals and readily undergo autoxidation with concomitant formation of 'active oxygen' species. These substances cause necrosis of striated muscle in rats, and it has been suggested that this is due to free radical formation and disruption of energy

Cardiolipin plays a role in KCN-induced necrosis.

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Cardiolipin (CL) is a unique anionic, dimeric phospholipid found almost exclusively in the inner mitochondrial membrane and is essential for the function of numerous enzymes that are involved in mitochondrial energy metabolism. While the role of cardiolipin in apoptosis is well established, its

75-kd sirtuin 1 blocks tumor necrosis factor α-mediated apoptosis in human osteoarthritic chondrocytes.

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OBJECTIVE Sirtuin 1 (SirT1) has been implicated in the regulation of human cartilage homeostasis and chondrocyte survival. Exposing human osteoarthritic (OA) chondrocytes to tumor necrosis factor α (TNFα) generates a stable and enzymatically inactive 75-kd form of SirT1 (75SirT1) via cathepsin

Metyrapone, an inhibitor of cytochrome oxidases, does not affect viability in a neuroblastoma cell model of bilirubin toxicity.

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BACKGROUND Unconjugated hyperbilirubinemia may cause brain damage in infants, and globally remains a source of neonatal morbidity and mortality. A significant inter-individual variability in vulnerability to bilirubin toxicity remains largely unexplained. An enzyme located in mitochondria oxidizes

[Activity of enzymes of the internal membrane of heart mitochondria and spectrum of blood fatty acids during myocardial necrosis reproduced after the stress].

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An increase of proton permeability, creation of the possibility for the superoxide radical O2-. to escape and a decrease in the oxidation rate of acetyl-CoA due to the stress origin with such membrane-bound enzymes as succinate dehydrogenase and cytochrome oxidase remaining as active as they were,

Peroxisome proliferator activated receptor-γ agonists protect oligodendrocyte progenitors against tumor necrosis factor-alpha-induced damage: Effects on mitochondrial functions and differentiation.

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The activation of the nuclear receptor peroxisome proliferator-activated receptor-γ (PPAR-γ) is known to exert anti-inflammatory and neuroprotective effects and PPAR-γ agonists are considered potential therapeutic agents in brain diseases including those affecting myelin. In demyelinating diseases

Toxicity testing of Senna occidentalis seed in rabbits.

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The effect was investigated of administering ground Senna occidentalis seeds to rabbits in different concentrations (1%, 2%, 3% and 4%) in the ration. The experiment lasted 30 days and the toxic effects of the plant were evaluated on the basis of weight gain, histopathological, biochemical and

Glycine maintains mitochondrial activity and bile composition following warm liver ischemia-reperfusion injury.

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OBJECTIVE Experimental studies have shown protective effect by the non-essential amino acid glycine to liver ischemia-reperfusion (I/R) injury but the mechanism of action is unknown. METHODS A rabbit model of hepatic lobar I/R was used. Three groups of animals (n=6) were studied: Sham group

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