Difference between revisions of "Hoffman 2007 Am J Physiol Heart Circ Physiol"
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{{Publication | {{Publication | ||
|title=Hoffman DL, Salter JD, Brookes PS (2007) Response of mitochondrial reactive oxygen species generation to steady-state oxygen tension: implications for hypoxic cell signaling. | |title=Hoffman DL, Salter JD, Brookes PS (2007) Response of mitochondrial reactive oxygen species generation to steady-state oxygen tension: implications for hypoxic cell signaling. Am J Physiol Heart Circ Physiol 292:H101-8. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16963616 PMID:16963616 Open Access] | |||
|authors=Hoffman DL, Salter JD, Brookes PS | |authors=Hoffman DL, Salter JD, Brookes PS | ||
|year=2007 | |year=2007 | ||
|journal= | |journal=Am J Physiol Heart Circ Physiol | ||
|abstract=Mitochondria are proposed to play an important role in hypoxic cell signaling. One currently accepted signaling paradigm is that the mitochondrial generation of reactive oxygen species (ROS) increases in hypoxia. This is paradoxical, because oxygen is a substrate for ROS generation. Although the response of isolated mitochondrial ROS generation to [O(2)] has been examined previously, such investigations did not apply rigorous control over [O(2)] within the hypoxic signaling range. With the use of open-flow respirometry and fluorimetry, the current study determined the response of isolated rat liver mitochondrial ROS generation to defined steady-state [O(2)] as low as 0.1 microM. In mitochondria respiring under state 4 (quiescent) or state 3 (ATP turnover) conditions, decreased ROS generation was always observed at low [O(2)]. It is concluded that the biochemical mechanism to facilitate increased ROS generation in response to hypoxia in cells is not intrinsic to the mitochondrial respiratory chain alone but may involve other factors. The implications for hypoxic cell signaling are discussed. | |abstract=Mitochondria are proposed to play an important role in hypoxic cell signaling. One currently accepted signaling paradigm is that the mitochondrial generation of reactive oxygen species (ROS) increases in hypoxia. This is paradoxical, because oxygen is a substrate for ROS generation. Although the response of isolated mitochondrial ROS generation to [O(2)] has been examined previously, such investigations did not apply rigorous control over [O(2)] within the hypoxic signaling range. With the use of open-flow respirometry and fluorimetry, the current study determined the response of isolated rat liver mitochondrial ROS generation to defined steady-state [O(2)] as low as 0.1 microM. In mitochondria respiring under state 4 (quiescent) or state 3 (ATP turnover) conditions, decreased ROS generation was always observed at low [O(2)]. It is concluded that the biochemical mechanism to facilitate increased ROS generation in response to hypoxia in cells is not intrinsic to the mitochondrial respiratory chain alone but may involve other factors. The implications for hypoxic cell signaling are discussed. | ||
|mipnetlab=US_MI_Ann_Arbor_Glick_GD | |mipnetlab=US_MI_Ann_Arbor_Glick_GD | ||
}} | }} | ||
* For a critical review on artefacts in oxygen kinetics in the paper by Hoffman et al (2007), see [[Scandurra_2010_Adv Exp Med Biol]]. | |||
== Cited by == | |||
{{Template:Cited by Komlodi 2021 MitoFit AmR-O2}} | |||
{{Template:Cited by Komlodi 2021 MitoFit AmR}} | |||
{{Template:Cited by Komlodi 2022 MitoFit ROS review}} | |||
{{Labeling | {{Labeling | ||
| | |area=Respiration | ||
|injuries= | |injuries=Oxidative stress;RONS | ||
|organism=Rat | |organism=Rat | ||
|tissues= | |tissues=Liver | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
|enzymes=Complex II; | |enzymes=Complex II;succinate dehydrogenase, Complex III | ||
| | |topics=Oxygen kinetics, Redox state | ||
| | |additional=MitoFit 2021 AmR-O2, MitoFit 2021 AmR, MitoFit 2022 ROS review | ||
}} | }} | ||
Latest revision as of 21:38, 13 April 2022
| Hoffman DL, Salter JD, Brookes PS (2007) Response of mitochondrial reactive oxygen species generation to steady-state oxygen tension: implications for hypoxic cell signaling. Am J Physiol Heart Circ Physiol 292:H101-8. |
Hoffman DL, Salter JD, Brookes PS (2007) Am J Physiol Heart Circ Physiol
Abstract: Mitochondria are proposed to play an important role in hypoxic cell signaling. One currently accepted signaling paradigm is that the mitochondrial generation of reactive oxygen species (ROS) increases in hypoxia. This is paradoxical, because oxygen is a substrate for ROS generation. Although the response of isolated mitochondrial ROS generation to [O(2)] has been examined previously, such investigations did not apply rigorous control over [O(2)] within the hypoxic signaling range. With the use of open-flow respirometry and fluorimetry, the current study determined the response of isolated rat liver mitochondrial ROS generation to defined steady-state [O(2)] as low as 0.1 microM. In mitochondria respiring under state 4 (quiescent) or state 3 (ATP turnover) conditions, decreased ROS generation was always observed at low [O(2)]. It is concluded that the biochemical mechanism to facilitate increased ROS generation in response to hypoxia in cells is not intrinsic to the mitochondrial respiratory chain alone but may involve other factors. The implications for hypoxic cell signaling are discussed.
• O2k-Network Lab: US_MI_Ann_Arbor_Glick_GD
- For a critical review on artefacts in oxygen kinetics in the paper by Hoffman et al (2007), see Scandurra_2010_Adv Exp Med Biol.
Cited by
- Komlódi T, Sobotka O, Gnaiger E (2021) Facts and artefacts on the oxygen dependence of hydrogen peroxide production using Amplex UltraRed. Bioenerg Commun 2021.4. https://doi:10.26124/BEC:2021-0004
- Komlódi T, Schmitt S, Zdrazilova L, Donnelly C, Zischka H, Gnaiger E. Oxygen dependence of hydrogen peroxide production in isolated mitochondria and permeabilized cells. MitoFit Preprints (in prep).
- Komlódi T, Gnaiger E (2022) Discrepancy on oxygen dependence of mitochondrial ROS production - review. MitoFit Preprints 2022 (in prep).
Labels: MiParea: Respiration
Stress:Oxidative stress;RONS Organism: Rat Tissue;cell: Liver Preparation: Isolated mitochondria Enzyme: Complex II;succinate dehydrogenase, Complex III Regulation: Oxygen kinetics, Redox state
MitoFit 2021 AmR-O2, MitoFit 2021 AmR, MitoFit 2022 ROS review
