Difference between revisions of "Aguirre 2012 Mitochondrion"
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{{Publication | {{Publication | ||
|title=Aguirre E, | |title=Aguirre E, Lopez-Bernardo E, Cadenas S (2012) Functional evidence for nitric oxide production by skeletal-muscle mitochondria from lipopolysaccharide-treated mice. Mitochondrion 12: 126-131. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21664300 PMID: 21664300] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/21664300 PMID: 21664300] | ||
|authors=Aguirre E, | |authors=Aguirre E, Lopez-Bernardo E, Cadenas S | ||
|year=2012 | |year=2012 | ||
|journal=Mitochondrion | |journal=Mitochondrion | ||
|abstract=The possible existence of a mitochondrially localized nitric oxide (NO) synthase (mtNOS) is controversial. To clarify this, we studied the ability of intact mitochondria to generate NO and the effect of mitochondrial NO on respiration. Respiratory rates and oxygen kinetics (P(50) values) were determined by high-resolution respirometry in skeletal-muscle mitochondria from control mice and mice injected with Escherichia coli lipopolysaccharide (LPS). In the presence of the NOS substrate L-arginine, mitochondria from LPS-treated mice had lower respiration rates and higher P(50) values than control animals. These effects were prevented by the NOS inhibitor L-NMMA. Our results suggest that mitochondrially derived NO is generated by an LPS-inducible NOS protein other than iNOS and modulates oxygen consumption in mouse skeletal muscle. | |abstract=The possible existence of a mitochondrially localized nitric oxide (NO) synthase (mtNOS) is controversial. To clarify this, we studied the ability of intact mitochondria to generate NO and the effect of mitochondrial NO on respiration. Respiratory rates and oxygen kinetics (P(50) values) were determined by high-resolution respirometry in skeletal-muscle mitochondria from control mice and mice injected with Escherichia coli lipopolysaccharide (LPS). In the presence of the NOS substrate L-arginine, mitochondria from LPS-treated mice had lower respiration rates and higher P(50) values than control animals. These effects were prevented by the NOS inhibitor L-NMMA. Our results suggest that mitochondrially derived NO is generated by an LPS-inducible NOS protein other than iNOS and modulates oxygen consumption in mouse skeletal muscle. | ||
|keywords=nitric oxide (NO) synthase (mtNOS), Respiratory rates and oxygen kinetics (P(50), Escherichia coli lipopolysaccharide (LPS) | |keywords=nitric oxide (NO) synthase (mtNOS), Respiratory rates and oxygen kinetics (P(50), Escherichia coli lipopolysaccharide (LPS) | ||
|mipnetlab=ES Madrid Cadenas S, | |mipnetlab=ES Madrid Cadenas S, | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
Revision as of 11:26, 17 April 2012
| Aguirre E, Lopez-Bernardo E, Cadenas S (2012) Functional evidence for nitric oxide production by skeletal-muscle mitochondria from lipopolysaccharide-treated mice. Mitochondrion 12: 126-131. |
Aguirre E, Lopez-Bernardo E, Cadenas S (2012) Mitochondrion
Abstract: The possible existence of a mitochondrially localized nitric oxide (NO) synthase (mtNOS) is controversial. To clarify this, we studied the ability of intact mitochondria to generate NO and the effect of mitochondrial NO on respiration. Respiratory rates and oxygen kinetics (P(50) values) were determined by high-resolution respirometry in skeletal-muscle mitochondria from control mice and mice injected with Escherichia coli lipopolysaccharide (LPS). In the presence of the NOS substrate L-arginine, mitochondria from LPS-treated mice had lower respiration rates and higher P(50) values than control animals. These effects were prevented by the NOS inhibitor L-NMMA. Our results suggest that mitochondrially derived NO is generated by an LPS-inducible NOS protein other than iNOS and modulates oxygen consumption in mouse skeletal muscle. • Keywords: nitric oxide (NO) synthase (mtNOS), Respiratory rates and oxygen kinetics (P(50), Escherichia coli lipopolysaccharide (LPS)
• O2k-Network Lab: ES Madrid Cadenas S
Labels:
Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Mouse Tissue;cell: Skeletal muscle Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
HRR: Oxygraph-2k
