Difference between revisions of "State 5"

Latest revision as of 11:18, 17 March 2019

high-resolution terminology - matching measurements at high-resolution

State 5

Description

State 5 is the respiratory state obtained in a protocol with isolated mitochondria after a sequence of State 1 to State 4, when the concentration of O₂ is depleted in the closed oxygraph chamber and zero oxygen (the anaerobic state) is reached (Chance and Williams, 1955; Table I).

State 5 is defined in the original publication in two ways: State 5 may be obtained by antimycin A treatment or by anaerobiosis (Chance and Williams, 1955; page 414). Antimycin A treatment yields a State 5 equivalent to a state for measurement of residual oxygen consumption, ROX (which may also be induced by rotenone+myxothiazol; Gnaiger 2009). Setting State 5 equivalent to ROX or anoxia (Chance and Williams 1955) can be rationalized only in the context of measurement of cytochrome redox states, whereas in the context of respiration State 5 is usually referred to as anoxic.

Reference: Chance 1955 JBC-III, Gnaiger 2009 Int J Biochem Cell Biol

MitoPedia concepts: Respiratory state, Find

MitoPedia topics: EAGLE

Communicated by Gnaiger E 2011-02-27, edited 2014-04-20.

State 5 and zero oxygen

State 5 after an aerobic-anoxic transition provides conditions for internal zero-oxygen calibration of the oxygen sensor under anoxia, which is essential for measurement of oxygen kinetics by high-resolution respirometry in a closed system (Gnaiger et al 1995; Scandurra and Gnaiger 2010). Although zero oxygen cannot strictly be reached owing to thermodynamic and kinetic contraints, a minimum p_O2 of 0.0003 kPa is calculated to be reached at typical mitochondrial incubation conditions, which is due to the high mitochondrial oxygen affinitiy and is practically zero from an experimental point of view (Gnaiger et al 1995). Owing to the low oxygen affinity of permeabilized muscle fibres (Gnaiger 2003), however, State 5 is difficult to be reached in such mt-preparations within tolerable short periods of incubation time.

References

Chance B, Williams GR (1955) Respiratory enzymes in oxidative phosphorylation. III. The steady state. J Biol Chem 217: 409-427.

Gnaiger E (2003) Oxygen conformance of cellular respiration. A perspective of mitochondrial physiology. Adv Exp Med Biol 543: 39-55. »Bioblast link«

Gnaiger E (2009) Capacity of oxidative phosphorylation in human skeletal muscle. New perspectives of mitochondrial physiology. Int J Biochem Cell Biol 41: 1837–1845. »Bioblast link«

Gnaiger E, Steinlechner-Maran R, Méndez G, Eberl T, Margreiter R (1995) Control of mitochondrial and cellular respiration by oxygen. J Bioenerg Biomembr 27: 583-596. »Bioblast link«

Scandurra FM, Gnaiger E (2010) Cell respiration under hypoxia: Facts and artefacts in mitochondrial oxygen kinetics. Adv Exp Med Biol 662: 7-25. »Bioblast link«

@@ Line 1: / Line 1: @@
 {{MitoPedia
-|abbr=n.a.
 |description='''State 5''' is the [[respiratory state]] obtained in a protocol with isolated mitochondria after a sequence of [[State 1]] to [[State 4]], when the concentration of O<sub>2</sub> is depleted in the closed oxygraph chamber and zero oxygen (the anaerobic state) is reached ([[Chance 1955 JBC-III|Chance and Williams, 1955]]; Table I).
-State 5 is defined in the original publication in two ways: ''State 5 may be obtained by antimycin A treatment or by anaerobiosis'' (Chance and Williams, 1955; page 414). [[Antimycin A]] treatment yields a State 5 equivalent to a state for measurement of [[residual oxygen consumption]], ROX (which may also be induced by [[rotenone]]+[[myxothiazol]]; [[Gnaiger_2009_IJBCB|Gnaiger 2009]]). Setting State 5 equivalent to ROX or anoxia (Chance and Williams 1955) can be rationalized only in the context of measurement of cytochrome redox states, whereas in the context of respiration State 5 is usually referred to as 'zero oxygen'.
+State 5 is defined in the original publication in two ways: ''State 5 may be obtained by antimycin A treatment or by anaerobiosis'' (Chance and Williams, 1955; page 414). [[Antimycin A]] treatment yields a State 5 equivalent to a state for measurement of [[residual oxygen consumption]], ROX (which may also be induced by [[rotenone]]+[[myxothiazol]]; [[Gnaiger 2009 Int J Biochem Cell Biol|Gnaiger 2009]]). Setting State 5 equivalent to ROX or anoxia (Chance and Williams 1955) can be rationalized only in the context of measurement of cytochrome redox states, whereas in the context of respiration State 5 is usually referred to as [[anoxic]].
-|info=[[Chance 1955 JBC-III]]; [[Gnaiger 2009 Int J Biochem Cell Biol]]
+|info=[[Chance 1955 JBC-III]], [[Gnaiger 2009 Int J Biochem Cell Biol]]
 }}
-{{MitoPedia methods
+{{MitoPedia concepts
-|mitopedia method=Respirometry, Spectrophotometry
+|mitopedia concept=Respiratory state, Find
 }}
 {{MitoPedia topics
-|mitopedia topic=Respiratory state
+|mitopedia topic=EAGLE
 }}
+ Communicated by [[Gnaiger E]] 2011-02-27, edited 2014-04-20.
 ==State 5 and zero oxygen==
-State 5 after an aerobic-anoxic transition provides conditions for internal zero-oxygen calibration of the oxygen sensor under [[anoxia]], which is essential for measurement of [[oxygen kinetics]] by [[high-resolution respirometry]] in a closed system ([[Gnaiger_1995_J Bioenerg Biomembr|Gnaiger et al 1995]]; [[Scandurra_2010_Adv Exp Med Biol|Scandurra and Gnaiger 2010]]). Although zero oxygen cannot strictly be reached owing to thermodynamic and kinetic contraints, a minimum ''p''<sub>O2</sub> of 0.0003 kPa is calculated to be reached at typical mitochondrial incubation conditions, which is due to the high mitochondrial oxygen affinitiy and is practically zero from an experimental point of view ([[Gnaiger_1995_JBB|Gnaiger et al 1995]]). Owing to the low oxygen affinity of permeabilized muscle fibres ([[Gnaiger_2003_Adv Exp Med Biol|Gnaiger 2003]]), however, State 5 is difficult to be reached in such mt-preparations within tolerable short periods of incubation time.
+:::: State 5 after an aerobic-anoxic transition provides conditions for internal zero-oxygen calibration of the oxygen sensor under [[anoxia]], which is essential for measurement of [[oxygen kinetics]] by [[high-resolution respirometry]] in a closed system ([[Gnaiger_1995_J_Bioenerg_Biomembr|Gnaiger et al 1995]]; [[Scandurra_2010_Adv Exp Med Biol|Scandurra and Gnaiger 2010]]). Although zero oxygen cannot strictly be reached owing to thermodynamic and kinetic contraints, a minimum ''p''<sub>O2</sub> of 0.0003 kPa is calculated to be reached at typical mitochondrial incubation conditions, which is due to the high mitochondrial oxygen affinitiy and is practically zero from an experimental point of view ([[Gnaiger_1995_J_Bioenerg_Biomembr|Gnaiger et al 1995]]). Owing to the low oxygen affinity of permeabilized muscle fibres ([[Gnaiger_2003_Adv Exp Med Biol|Gnaiger 2003]]), however, State 5 is difficult to be reached in such mt-preparations within tolerable short periods of incubation time.
 == References ==
-Chance B, Williams GR (1955) Respiratory enzymes in oxidative phosphorylation. III. The steady state. J Biol Chem 217: 409-427.
+::::* Chance B, Williams GR (1955) Respiratory enzymes in oxidative phosphorylation. III. The steady state. J Biol Chem 217: 409-427.
-Gnaiger E (2003) Oxygen conformance of cellular respiration. A perspective of mitochondrial physiology. Adv Exp Med Biol 543: 39-55. [[Gnaiger_2003_Adv Exp Med Biol|PMID: 8746845]]
+::::* Gnaiger E (2003) Oxygen conformance of cellular respiration. A perspective of mitochondrial physiology. Adv Exp Med Biol 543: 39-55. [[Gnaiger_2003_Adv Exp Med Biol|»Bioblast link«]]
-Gnaiger E (2009) Capacity of oxidative phosphorylation in human skeletal muscle. New perspectives of mitochondrial physiology. Int J Biochem Cell Biol 41: 1837–1845. [[Gnaiger 2009 Int J Biochem Cell Biol|PMID: 19467914]]
+::::* Gnaiger E (2009) Capacity of oxidative phosphorylation in human skeletal muscle. New perspectives of mitochondrial physiology. Int J Biochem Cell Biol 41: 1837–1845. [[Gnaiger 2009 Int J Biochem Cell Biol|»Bioblast link«]]
-Gnaiger E, Steinlechner-Maran R, Méndez G, Eberl T, Margreiter R (1995) Control of mitochondrial and cellular respiration by oxygen. J Bioenerg Biomembr 27: 583-596. [[Gnaiger_1995_J Bioenerg Biomembr|PMID: 14713113]]
+::::* Gnaiger E, Steinlechner-Maran R, Méndez G, Eberl T, Margreiter R (1995) Control of mitochondrial and cellular respiration by oxygen. J Bioenerg Biomembr 27: 583-596. [[Gnaiger_1995_J_Bioenerg_Biomembr|»Bioblast link«]]
-Scandurra FM, Gnaiger E (2010) Cell respiration under hypoxia: Facts and artefacts in mitochondrial oxygen kinetics. Adv Exp Med Biol 662: 7-25. [[Scandurra_2010_Adv Exp Med Biol|PMID: 20204766]]
+::::* Scandurra FM, Gnaiger E (2010) Cell respiration under hypoxia: Facts and artefacts in mitochondrial oxygen kinetics. Adv Exp Med Biol 662: 7-25. [[Scandurra_2010_Adv Exp Med Biol |»Bioblast link«]]