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Difference between revisions of "Lee 1996 Biol Bull"

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{{Publication
{{Publication
|title=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.
|title=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 191:421-30.
|authors=Lee RW, Kraus DW, Doeller JE Β 
|info=[http://www.biolbull.org/cgi/reprint/191/3/421?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=kraus&searchid=1&FIRSTINDEX=0&volume=191&issue=3&resourcetype=HWCIT Biol. Bull. 191: 421-430.]
|authors=Lee RW, Kraus DW, Doeller JE
|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 (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.
|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''.
Β 
|mipnetlab=US AL Birmingham Kraus DW
Β 
|discipline=Mitochondrial Physiology
|info=[http://www.biolbull.org/cgi/reprint/191/3/421?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=kraus&searchid=1&FIRSTINDEX=0&volume=191&issue=3&resourcetype=HWCIT Biol. Bull. 191: 421-430.]
}}
}}
{{Labeling
{{Labeling
|area=Respiration, Comparative MiP;environmental MiP
|organism=Molluscs
|tissues=Lung;gill
|enzymes=Complex IV;cytochrome c oxidase
|topics=Redox state
|couplingstates=OXPHOS
|instruments=Oxygraph-2k
|discipline=Mitochondrial Physiology
|discipline=Mitochondrial Physiology
|organism=Yeast; Fungi
|enzymes=Complex IV; Cytochrome c Oxidase
|topics=Respiration; OXPHOS; ETS Capacity, Flux Control; Additivity; Threshold; Excess Capacity
|instruments=Oxygraph-2k
}}
}}

Latest revision as of 10:07, 9 November 2016

Publications in the MiPMap
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 191:421-30.

Β» 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.


β€’ O2k-Network Lab: US AL Birmingham Kraus DW


Labels: MiParea: Respiration, Comparative MiP;environmental MiP 


Organism: Molluscs  Tissue;cell: Lung;gill 

Enzyme: Complex IV;cytochrome c oxidase  Regulation: Redox state  Coupling state: OXPHOS 

HRR: Oxygraph-2k