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Mitochondrial Cytochrome C Oxidase (mitochondrial + cytochrome_c_oxidase)
Terms modified by Mitochondrial Cytochrome C Oxidase Selected AbstractsCaligus elongatus Nordmann genotypes on wild and farmed fishJOURNAL OF FISH DISEASES, Issue 2 2007Ø Øines Abstract Two mitochondrial genotypes have been described for Caligus elongatus Nordmann in Norway. This article reports on the distribution of C. elongatus mitochondrial cytochrome C oxidase 1 genotypes from wild fish hosts from the SE Norwegian coast. For comparison, lice from areas with fish farming were included in the study. The genotype distribution of 841 lice from wild coastal (n = 535), wild North Sea pelagic (n = 26), farmed (n = 160) and wild hosts in areas of fish farming (n = 89) is presented. The genotype frequencies of C. elongatus on wild coastal hosts varied significantly between spring and autumn. Lice from these fish show a large proportion of genotype 1 lice in March,June every year. Genotype 2 lice were found more frequently in autumn. Genotype 1 was clearly associated with the lumpfish, Cyclopterus lumpus L. The genotype frequency appeared to be different in areas with aquaculture. Caligus elongatus from farmed fish and wild fish caught close to Atlantic salmon fish farms in Norway were predominantly genotype 1 in autumn. Genotypes of C. elongatus on the SE coast of Norway vary according to season and fish species. Factors involved in the encounter between fish and lice are important for the establishment of lice on their hosts. [source] Sulfide : quinone oxidoreductase (SQR) from the lugworm Arenicola marina shows cyanide- and thioredoxin-dependent activityFEBS JOURNAL, Issue 6 2008Ursula Theissen The lugworm Arenicola marina inhabits marine sediments in which sulfide concentrations can reach up to 2 mm. Although sulfide is a potent toxin for humans and most animals, because it inhibits mitochondrial cytochrome c oxidase at micromolar concentrations, A. marina can use electrons from sulfide for mitochondrial ATP production. In bacteria, electron transfer from sulfide to quinone is catalyzed by the membrane-bound flavoprotein sulfide : quinone oxidoreductase (SQR). A cDNA from A. marina was isolated and expressed in Saccharomyces cerevisiae, which lacks endogenous SQR. The heterologous enzyme was active in mitochondrial membranes. After affinity purification, Arenicola SQR isolated from yeast mitochondria reduced decyl-ubiquinone (Km = 6.4 ,m) after the addition of sulfide (Km = 23 ,m) only in the presence of cyanide (Km = 2.6 mm). The end product of the reaction was thiocyanate. When cyanide was substituted by Escherichia coli thioredoxin and sulfite, SQR exhibited one-tenth of the cyanide-dependent activity. Six amino acids known to be essential for bacterial SQR were exchanged by site-directed mutagenesis. None of the mutant enzymes was active after expression in yeast, implicating these amino acids in the catalytic mechanism of the eukaryotic enzyme. [source] Cytochrome c oxidase as the target of the heat shock protective effect in septic liverINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 5 2004Hsiang-Wen Chen Summary Liver function failure is one of the characteristics of critically ill, septic patients and is associated with worse outcome. Our previous studies have demonstrated that heat-shock response protects cells and tissue from subsequent insults and improves survival during sepsis. In this study, we have shown that mitochondrial cytochrome c oxidase (CCO) is one of the major sources of that protective effect. Experimental sepsis was induced by the cecal ligation and puncture (CLP) method. Heat-shock treatment was induced in rats by hyperthermia 24 h before CLP operation. The results showed that ATP content of the liver declined significantly, and the enzymatic activity of mitochondrial CCO was apparently suppressed during the late stages of sepsis. The mitochondrial ultrastructure of septic liver showed the deformity, mild swelling and inner membrane budding. Heat-shock treatment led to heat-shock protein 72 overexpression and prevented the downregulation of Grp75 during sepsis. On the contrary, the expression of the enzyme complex and its activity were preserved, associated with the minimization of ultrastructural deformities. In conclusion, the maintenance of mitochondrial function, especially the CCO, may be an important strategy in therapeutic interventions of a septic liver. [source] DNA barcodes to identify species and explore diversity in the Adelgidae (Insecta: Hemiptera: Aphidoidea)MOLECULAR ECOLOGY RESOURCES, Issue 2009R. G. FOOTTIT Abstract The Adelgidae are relatively small, cryptic insects, exhibiting complex life cycles with parthenogenetic reproduction. Due to these characteristics, the taxonomy of the group is problematic. Here, we test the effectiveness of the standard 658-bp barcode fragment from the 5,-end of the mitochondrial cytochrome c oxidase 1 gene (COI) in differentiating among 17 species of Adelgidae, in associating life-cycle stages, and in assessing patterns of geographical variation in selected species. Species of Adelgidae are well-differentiated by DNA barcodes, enabling the identification of different morphological forms, immature stages and individuals on different hosts and at different periods of the life cycle. DNA barcodes have uncovered cryptic diversity within taxa and, in other cases, a lack of sequence divergence in species pairs previously separated by life-cycle characteristics, indicating a need for further taxonomic analysis. [source] Species identification of aphids (Insecta: Hemiptera: Aphididae) through DNA barcodesMOLECULAR ECOLOGY RESOURCES, Issue 6 2008R. G. FOOTTIT Abstract A 658-bp fragment of mitochondrial DNA from the 5, region of the mitochondrial cytochrome c oxidase 1 (COI) gene has been adopted as the standard DNA barcode region for animal life. In this study, we test its effectiveness in the discrimination of over 300 species of aphids from more than 130 genera. Most (96%) species were well differentiated, and sequence variation within species was low, averaging just 0.2%. Despite the complex life cycles and parthenogenetic reproduction of aphids, DNA barcodes are an effective tool for identification. [source] Mitochondrial impacts of insecticidal formate esters in insecticide-resistant and insecticide-susceptible Drosophila melanogasterPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 6 2009Cheol Song Abstract BACKGROUND: Previous research on insecticidal formate esters in flies and mosquitoes has documented toxicity profiles, metabolism characteristics and neurological impacts. The research presented here investigated mitochondrial impacts of insecticidal formate esters and their hydrolyzed metabolite formic acid in the model dipteran insect Drosophila melanogaster Meig. These studies compared two Drosophila strains: an insecticide-susceptible strain (Canton-S) and a strain resistant by cytochrome P450 overexpression (Hikone-R). RESULTS: In initial studies investigating inhibition of mitochondrial cytochrome c oxidase, two proven insecticidal materials (hydramethylnon and sodium cyanide) caused significant inhibition. However, for insecticidal formate esters and formic acid, no significant inhibition was identified in either fly strain. Mitochondrial impacts of formate esters were then investigated further by tracking toxicant-induced cytochrome c release from mitochondria into the cytoplasm, a biomarker of apoptosis and neurological dysfunction. Formic acid and three positive control treatments (rotenone, antimycin A and sodium cyanide) induced cytochrome c release, verifying that formic acid is capable of causing mitochondrial disruption. However, when comparing formate ester hydrolysis and cytochrome c release between Drosophila strains, formic acid liberation was only weakly correlated with cytochrome c release in the susceptible Canton-S strain (r2 = 0.70). The resistant Hikone-R strain showed no correlation (r2 < 0.0001) between formate ester hydrolysis and cytochrome c release. CONCLUSION: The findings of this study provide confirmation of mitochondrial impacts by insecticidal formate esters and suggest links between mitochondrial disruption, respiratory inhibition, apoptosis and formate-ester-induced neurotoxicity. Copyright © 2009 Society of Chemical Industry [source] Introduction on the multifaceted roles of nitric oxide in the retinaACTA OPHTHALMOLOGICA, Issue 2009NN OSBORNE Multifaceted roles of nitric oxide in the retina. N.N. Osborne. Nuffield Lab of Ophthalmology, University of Oxford, Oxford, United Kingdom Nitric oxide (NO), a free radical gas with a half-life of a few seconds is implicated in various physiological and pathophysiological roles associated with the retina and its vasculature. Generated by a family of nitric oxide synthetases (NOS), NO has been shown to bind to soluble guanylyl cyclase and to mitochondrial cytochrome c oxidase to activate defined signalling cascades. Different types of NOS exist and can be activated by calcium dependent (NOS1 and NOS3) or independent (NOS2) mechanisms. Generally, NOS1 is located to neurones while NOS2 and NOS3 are in glial and endothelial cells, respectively. NO is involved in communication between different neurones, glial cells and neurones, and in the interactions of endothelial cells with pericytes and neurones. As a consequence, a reduction in the generation of endogenous NO in the healthy retina can result in vasoconstriction; the consequences of such an affect on the retina and alterations in visual processing may alter the photoreceptor transduction mechanism and communication between retinal cells. The binding of NO to mitochondrial cytochrome c oxidase to effectively compete with oxygen has been suggested be involved in a number of processes. NO-elicited events act as triggers by which mitochondrial signal transduction cascades become involved in the induction of cellular defence mechanisms and adaptive responses. Moreover, the effect of NO on the electron transport chain might lead to mitochondrial dysfunction and pathology. NO clearly has a multifaceted role in the healthy and unhealthy retina. [source] | |||||||||||||