Difference between revisions of "Lee 1996 Biol Bull"
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|year=1996 | |year=1996 | ||
|journal=Biol Bull | |journal=Biol Bull | ||
|abstract=Organisms, such as the mussel ''Geukensia demissa'', that inhabit high-sulfide sediments have mechanisms that impede sulfide poisoning of aerobic respiration. Oxygen consumption rates (nO<sub>2</sub>) of excised ciliated gills from freshly collected ''G. demissa'' were stimulated 3-fold at sulfide concentrations between 200 and 500 {mu}M and remained stimulated at 1000 {mu}M. Maintenance of mussels in sulfide-free conditions resulted in less stimulation of gill nO<sub>2</sub> at <500 {mu}M sulfide and inhibition between 500 and 1000 {mu}M sulfide. Gills of ''Mytilus galloprovincialis'' from a sulfide-free environment were inhibited by {ge}200 {mu}M sulfide. These results indicate that sulfide stimulation of nO2 may be correlated to environmental exposure to sulfide. Serotonin, a neurohormonal stimulant of ciliary beating, further increased sulfide-stimulated nO<sub>2</sub>, possibly in support of energy demand. Sulfide-stimulated | |abstract=Organisms, such as the mussel ''Geukensia demissa'', that inhabit high-sulfide sediments have mechanisms that impede sulfide poisoning of aerobic respiration. Oxygen consumption rates (nO<sub>2</sub>) of excised ciliated gills from freshly collected ''G. demissa'' were stimulated 3-fold at sulfide concentrations between 200 and 500 {mu}M and remained stimulated at 1000 {mu}M. Maintenance of mussels in sulfide-free conditions resulted in less stimulation of gill nO<sub>2</sub> at <500 {mu}M sulfide and inhibition between 500 and 1000 {mu}M sulfide. Gills of ''Mytilus galloprovincialis'' from a sulfide-free environment were inhibited by {ge}200 {mu}M sulfide. These results indicate that sulfide stimulation of nO2 may be correlated to environmental exposure to sulfide. Serotonin, a neurohormonal stimulant of ciliary beating, further increased sulfide-stimulated nO<sub>2</sub>, possibly in support of energy demand. Sulfide-stimulated nO<sub>2</sub> was negligible in boiled gills and was 61% inhibited by cyanide, implicating the participation of mitochondrial electron flux. Mitochondrial cytochromes c and oxidase oxidation/ reduction state changed little at <500 {mu}M sulfide, but reduction occurred at 500-2000 {mu}M sulfide, suggesting that although cytochrome oxidation/reduction state may be regulated in the face of increased electron flux, regulation may fail at inhibitory sulfide levels. Sulfide-stimulated nO<sub>2</sub> may represent a detoxification mechanism in ''G. demissa''. | ||
|mipnetlab=US AL Birmingham Kraus DW | |mipnetlab=US AL Birmingham Kraus DW | ||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology | ||
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{{Labeling | {{Labeling | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
| | |taxonomic group=Molluscs | ||
|tissues=Lung | |tissues=Lung; Gill | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|enzymes=Complex IV; Cytochrome c Oxidase | |enzymes=Complex IV; Cytochrome c Oxidase | ||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology | ||
}} | }} | ||
Revision as of 14:08, 11 March 2013
| Lee RW, Kraus DW, Doeller JE (1996) Sulfide-stimulation of oxygen consumption rate and cytochrome reduction in gills of the estuarine mussel Geukensia demissa. Biol Bull 191: 421-430. |
Lee RW, Kraus DW, Doeller JE (1996) Biol Bull
Abstract: Organisms, such as the mussel Geukensia demissa, that inhabit high-sulfide sediments have mechanisms that impede sulfide poisoning of aerobic respiration. Oxygen consumption rates (nO2) of excised ciliated gills from freshly collected G. demissa were stimulated 3-fold at sulfide concentrations between 200 and 500 {mu}M and remained stimulated at 1000 {mu}M. Maintenance of mussels in sulfide-free conditions resulted in less stimulation of gill nO2 at <500 {mu}M sulfide and inhibition between 500 and 1000 {mu}M sulfide. Gills of Mytilus galloprovincialis from a sulfide-free environment were inhibited by {ge}200 {mu}M sulfide. These results indicate that sulfide stimulation of nO2 may be correlated to environmental exposure to sulfide. Serotonin, a neurohormonal stimulant of ciliary beating, further increased sulfide-stimulated nO2, possibly in support of energy demand. Sulfide-stimulated nO2 was negligible in boiled gills and was 61% inhibited by cyanide, implicating the participation of mitochondrial electron flux. Mitochondrial cytochromes c and oxidase oxidation/ reduction state changed little at <500 {mu}M sulfide, but reduction occurred at 500-2000 {mu}M sulfide, suggesting that although cytochrome oxidation/reduction state may be regulated in the face of increased electron flux, regulation may fail at inhibitory sulfide levels. Sulfide-stimulated nO2 may represent a detoxification mechanism in G. demissa.
• O2k-Network Lab: US AL Birmingham Kraus DW
Labels:
Tissue;cell: Lung; Gill"Lung; Gill" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Enzyme: Complex IV; Cytochrome c Oxidase"Complex IV; Cytochrome c Oxidase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property.
Coupling state: OXPHOS
HRR: Oxygraph-2k
