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Difference between revisions of "Kupsch 2009 FEBS J"

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(Created page with "{{Publication |title=Kupsch K, Hertel S, Kreutzmann P, Wolf G, Wallesch CW, Siemen D, Schönfeld P (2009) Impairment of mitochondrial function by minocycline. FEBS J. 276: 1729...")
 
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depolarization and a decrease in state 3 as well as uncoupled
depolarization and a decrease in state 3 as well as uncoupled
respiration. Swelling of RLM in KCl-based medium indicates that MC permeabilizes
respiration. Swelling of RLM in KCl-based medium indicates that MC permeabilizes
the inner mitochondrial membrane (IMM) to K+ and Cl). This
the inner mitochondrial membrane (IMM) to K<sup>+</sup> and Cl). This
view is supported by our findings that MC-induced swelling in the KClbased
view is supported by our findings that MC-induced swelling in the KClbased
medium was partly suppressed by N,N¢-dicyclohexylcarbodiimide (an
medium was partly suppressed by N,N¢-dicyclohexylcarbodiimide (an
inhibitor of IMM-linked K+-transport) and tributyltin (an inhibitor of the
inhibitor of IMM-linked K<sup>+</sup>-transport) and tributyltin (an inhibitor of the
inner membrane anion channel) and that swelling was less pronounced
inner membrane anion channel) and that swelling was less pronounced
when RLM were suspended in choline chloride-based medium. In addition,
when RLM were suspended in choline chloride-based medium. In addition,
we observed a rapid MC-induced depletion of endogenous Mg2+ from
we observed a rapid MC-induced depletion of endogenous Mg<sup>2+</sup> from
RLM, an event that is known to activate ion-conducting pathways within
RLM, an event that is known to activate ion-conducting pathways within
the IMM. Moreover, MC abolished the Ca2+ retention capacity of RLM
the IMM. Moreover, MC abolished the Ca<sup>2+</sup> retention capacity of RLM
irrespective of the incubation medium used, most likely by triggering permeability
irrespective of the incubation medium used, most likely by triggering permeability
transition. In summary, we found that MC at low micromolar
transition. In summary, we found that MC at low micromolar
concentrations impairs several energy-dependent functions of mitochondria
concentrations impairs several energy-dependent functions of mitochondria
in vitro.
''in vitro''.
|keywords=Magnesium, Minocycline, Mitochondria, Neuroprotection, Permeability transition
|keywords=Magnesium, Minocycline, Mitochondria, Neuroprotection, Permeability transition
}}
}}

Revision as of 10:37, 2 November 2010

Publications in the MiPMap
Kupsch K, Hertel S, Kreutzmann P, Wolf G, Wallesch CW, Siemen D, Schönfeld P (2009) Impairment of mitochondrial function by minocycline. FEBS J. 276: 1729–1738.


Kupsch K, Hertel S, Kreutzmann P, Wolf G, Wallesch CW, Siemen D, Schoenfeld P (2009) FEBS J.

Abstract: There is an ongoing debate on the presence of beneficial effects of minocycline (MC), a tetracycline-like antibiotic, on the preservation of mitochondrial functions under conditions promoting mitochondria-mediated apoptosis. Here, we present a multiparameter study on the effects of MC on isolated rat liver mitochondria (RLM) suspended either in a KCl-based or in a sucrose-based medium. We found that the incubation medium used strongly affects the response of RLM to MC. In KCl-based medium, but not in sucrose-based medium, MC triggered mitochondrial swelling and cytochrome c release. MC-dependent swelling was associated with mitochondrial depolarization and a decrease in state 3 as well as uncoupled respiration. Swelling of RLM in KCl-based medium indicates that MC permeabilizes the inner mitochondrial membrane (IMM) to K+ and Cl). This view is supported by our findings that MC-induced swelling in the KClbased medium was partly suppressed by N,N¢-dicyclohexylcarbodiimide (an inhibitor of IMM-linked K+-transport) and tributyltin (an inhibitor of the inner membrane anion channel) and that swelling was less pronounced when RLM were suspended in choline chloride-based medium. In addition, we observed a rapid MC-induced depletion of endogenous Mg2+ from RLM, an event that is known to activate ion-conducting pathways within the IMM. Moreover, MC abolished the Ca2+ retention capacity of RLM irrespective of the incubation medium used, most likely by triggering permeability transition. In summary, we found that MC at low micromolar concentrations impairs several energy-dependent functions of mitochondria in vitro. Keywords: Magnesium, Minocycline, Mitochondria, Neuroprotection, Permeability transition


Labels:

Stress:Cancer; Apoptosis; Cytochrome c"Cancer; Apoptosis; Cytochrome c" 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: Rat  Tissue;cell: Hepatocyte; Liver"Hepatocyte; Liver" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.  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. 

Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Coupling; Membrane Potential"Coupling; Membrane Potential" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. 


HRR: Oxygraph-2k