Difference between revisions of "Thiede 2012 Biochim Biophys Acta"
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{{Publication | {{Publication | ||
|title=Thiede A, Gellerich FN, | |title=Thiede A, Gellerich FN, Schönfeld P, Siemen D (2012) Complex effects of 17β-estradiol on mitochondrial function. Biochim Biophys Acta 1817:1747-53. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/22414665 PMID: 22414665] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/22414665 PMID: 22414665 Open Access] | ||
|authors=Thiede A, Gellerich FN, Schoenfeld P, Siemen D | |authors=Thiede A, Gellerich FN, Schoenfeld P, Siemen D | ||
|year=2012 | |year=2012 | ||
| Line 7: | Line 7: | ||
|abstract=Existing literature on estradiol indicates that it affects mitochondrial functions at low micromolar concentrations. Particularly blockade of the permeability transition pore (PTP) or modulation of the enzymatic activity of one or more complexes of the respiratory chain were suspicious. We prepared mitoplasts from rat liver mitochondria (RLM) to study by single-channel patch-clamp techniques the PTP, and from rat astrocytes to study the potassium BK-channel said to modulate the PTP. Additionally, we measured respiration of intact RLM. After application of 17β-estradiol (βE) our single-channel results reveal a transient increase of activity of both, the BK-channel and the PTP followed by their powerful inhibition. Respiration measurements demonstrate inhibition of the Ca(2+)-induced permeability transition, as well, though only at higher concentrations (≥30μM). At lower concentrations, we observed an increase of endogenous- and state 2-respiration. Furthermore, we show that βE diminishes the phosphorylating respiration supported by complex I-substrates (glutamate/malate) or by the complex II-substrate succinate. Taken together the results suggest that βE affects mitochondria by several modes, including partial inhibition of the activities of ion channels of the inner membrane and of respiration. | |abstract=Existing literature on estradiol indicates that it affects mitochondrial functions at low micromolar concentrations. Particularly blockade of the permeability transition pore (PTP) or modulation of the enzymatic activity of one or more complexes of the respiratory chain were suspicious. We prepared mitoplasts from rat liver mitochondria (RLM) to study by single-channel patch-clamp techniques the PTP, and from rat astrocytes to study the potassium BK-channel said to modulate the PTP. Additionally, we measured respiration of intact RLM. After application of 17β-estradiol (βE) our single-channel results reveal a transient increase of activity of both, the BK-channel and the PTP followed by their powerful inhibition. Respiration measurements demonstrate inhibition of the Ca(2+)-induced permeability transition, as well, though only at higher concentrations (≥30μM). At lower concentrations, we observed an increase of endogenous- and state 2-respiration. Furthermore, we show that βE diminishes the phosphorylating respiration supported by complex I-substrates (glutamate/malate) or by the complex II-substrate succinate. Taken together the results suggest that βE affects mitochondria by several modes, including partial inhibition of the activities of ion channels of the inner membrane and of respiration. | ||
|keywords=Permeability transition pore (PTP), 17β-estradiol | |keywords=Permeability transition pore (PTP), 17β-estradiol | ||
|mipnetlab=DE Magdeburg Gellerich FN, DE Magdeburg Siemen D, DE Magdeburg | |mipnetlab=DE Magdeburg Gellerich FN, DE Magdeburg Siemen D, DE Magdeburg Schoenfeld P | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Rat | |organism=Rat | ||
|tissues=Nervous system, Liver | |tissues=Nervous system, Liver | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
|couplingstates=LEAK, OXPHOS, | |enzymes=Complex I, Complex II;succinate dehydrogenase | ||
| | |couplingstates=LEAK, OXPHOS, ET | ||
|instruments=Oxygraph-2k | |||
}} | }} | ||
* This article is part of a Special Issue entitled: 17th European Bioenergetics Conference ([http://www.ebec2012.uni-freiburg.de/ EBEC 2012]). | * This article is part of a Special Issue entitled: 17th European Bioenergetics Conference ([http://www.ebec2012.uni-freiburg.de/ EBEC 2012]). | ||
== Correction == | |||
An Oroboros Oxygraph-2k was used in this publication, whereas the Anton Paar/Oroboros Oxygraph was the first-generation instrument for high-resolution respirometry, which was replaced by the Oxygraph-2k in 2002. | |||
* ''Further details'': [[Gnaiger 2012 Abstract Bioblast-Gentle Science]] | |||
Latest revision as of 10:59, 23 January 2019
| Thiede A, Gellerich FN, Schönfeld P, Siemen D (2012) Complex effects of 17β-estradiol on mitochondrial function. Biochim Biophys Acta 1817:1747-53. |
Thiede A, Gellerich FN, Schoenfeld P, Siemen D (2012) Biochim Biophys Acta
Abstract: Existing literature on estradiol indicates that it affects mitochondrial functions at low micromolar concentrations. Particularly blockade of the permeability transition pore (PTP) or modulation of the enzymatic activity of one or more complexes of the respiratory chain were suspicious. We prepared mitoplasts from rat liver mitochondria (RLM) to study by single-channel patch-clamp techniques the PTP, and from rat astrocytes to study the potassium BK-channel said to modulate the PTP. Additionally, we measured respiration of intact RLM. After application of 17β-estradiol (βE) our single-channel results reveal a transient increase of activity of both, the BK-channel and the PTP followed by their powerful inhibition. Respiration measurements demonstrate inhibition of the Ca(2+)-induced permeability transition, as well, though only at higher concentrations (≥30μM). At lower concentrations, we observed an increase of endogenous- and state 2-respiration. Furthermore, we show that βE diminishes the phosphorylating respiration supported by complex I-substrates (glutamate/malate) or by the complex II-substrate succinate. Taken together the results suggest that βE affects mitochondria by several modes, including partial inhibition of the activities of ion channels of the inner membrane and of respiration. • Keywords: Permeability transition pore (PTP), 17β-estradiol
• O2k-Network Lab: DE Magdeburg Gellerich FN, DE Magdeburg Siemen D, DE Magdeburg Schoenfeld P
Labels:
Organism: Rat
Tissue;cell: Nervous system, Liver
Preparation: Isolated mitochondria
Enzyme: Complex I, Complex II;succinate dehydrogenase
Coupling state: LEAK, OXPHOS, ET
HRR: Oxygraph-2k
- This article is part of a Special Issue entitled: 17th European Bioenergetics Conference (EBEC 2012).
Correction
An Oroboros Oxygraph-2k was used in this publication, whereas the Anton Paar/Oroboros Oxygraph was the first-generation instrument for high-resolution respirometry, which was replaced by the Oxygraph-2k in 2002.
- Further details: Gnaiger 2012 Abstract Bioblast-Gentle Science
