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We began analyzing https://link.springer.com/article/10.1007/s11010-005-9066-6, but it redirected us to https://link.springer.com/article/10.1007/s11010-005-9066-6. The analysis below is for the second page.

Title[redir]:
Diazoxide-induced respiratory inhibition – a putative mitochondrial KATP channel independent mechanism of pharmacological preconditioning | Molecular and Cellular Biochemistry
Description:
The ischemic preconditioning biological phenomenon has been explored to identify putative pharmacologic agents to mimic this cytoprotective program against cellular ischemic injury. Diazoxide administration confers this cytoprotection, however, whether this is via direct activation of the putative mitochondrial KATP (mKATP) channel which was originally proposed has been questioned. Here, we present data supporting an alternate hypothesis evoking mitochondrial respiratory inhibition rather than mKATP channel activation, as a mediating event in the diazoxide-activated cytoprotective program. Mitochondrial respiration and reactive oxygen species (ROS) production was measured in digitonin-permeabilized C2C12 myotubes, allowing for the modulation of mKATP conductance by changing the potassium concentration of the medium (0–130 mM). Diazoxide dose-dependently attenuated succinate-supported respiration, an effect that was independent of mKATP channel conductance. Similarly, 5-hydroxydecanoate (5-HD), a putative mKATP channel blocker, released diazoxide-induced respiratory inhibition independently of potassium concentration. Since diazoxide-induced cytoprotection and respiratory inhibition are both integrally linked to ROS generation we repeated above experiments following ROS generation using DCF fluorescence. Cytoprotective doses of diazoxide increased ROS generation independently of potassium concentration and 5-HD inhibited ROS production under the same conditions. Collectively these data support the hypothesis that diazoxide-mediated cytoprotection is independent of the conductance of the mKATP channel and rather implicate mitochondrial respiratory inhibition-triggered ROS signaling.

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Keywords {🔍}

cas, google, scholar, pubmed, article, mitochondrial, channel, preconditioning, physiol, circ, katp, diazoxide, mitochondria, channels, res, ischemic, heart, cell, inhibition, potassium, respiratory, reactive, oxygen, rat, sack, species, generation, mechanism, mkatp, ros, atpsensitive, cardioprotection, diazoxideinduced, putative, minners, yellon, access, biol, privacy, cookies, content, data, research, respiration, hydroxydecanoate, signaling, opening, mol, publish, search,

Topics {✒️}

diazoxide/glibencamide-sensitive katp channels month download article/chapter digitonin-permeabilized c2c12 myotubes targeting nucleotide-requiring enzymes da silva mm atp-sensitive potassium channel reactive oxygen species nitric oxide-induced protection post-ischemic reperfused heart heart-derived cell line enhance drug-induced apoptosis classical ischemic preconditioning-moving diazoxide-activated cytoprotective program vascular reactive species full article pdf adult rat myocytes mitochondrial katp channels putative mitochondrial katp digitonin-permeabilized cells garlid kd prevents respiratory impairment cellular biochemistry aims mitochondrial katp channel cardiac katp channel selective chemical inhibition privacy choices/manage cookies respiratory inhibition mitochondrial atp-sensitive mitochondrial atp- sensitive pancreatic b-cells human leukemia cells redox- sensitive mechanism article minners dzeja pp diazoxide-induced cardioprotection mitochondrial redox signaling trimetazidine modulate preconditioning diazoxide-induced cytoprotection ros-mediated mechanism diazoxide administration confers reactive oxygen isolated rat heart perfused rat heart redox-based mechanism cellular ischemic injury + oxidation-reduction state channels triggers cardioprotection article molecular van wylen dg hypoxia induce preconditioning

Questions {❓}

Are reactive oxygen species involved?
Hausenloy DJ, Maddock HL, Baxter GF, Yellon DM: Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning?
Liu Y, Sato T, O'Rourke B, Marban E: Mitochondrial ATP-dependent potassium channels: novel effectors of cardioprotection?
Moncada S, Erusalimsky JD: Does nitric oxide modulate mitochondrial energy generation and apoptosis?
Ovide-Bordeaux S, Ventura-Clapier R, Veksler V: Do modulators of the mitochondrial K(ATP) channel change the function of mitochondria in situ?
Szewczyk A, Marban E: Mitochondria: a new target for K channel openers?

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         description:The ischemic preconditioning biological phenomenon has been explored to identify putative pharmacologic agents to mimic this cytoprotective program against cellular ischemic injury. Diazoxide administration confers this cytoprotection, however, whether this is via direct activation of the putative mitochondrial KATP (mKATP) channel which was originally proposed has been questioned. Here, we present data supporting an alternate hypothesis evoking mitochondrial respiratory inhibition rather than mKATP channel activation, as a mediating event in the diazoxide-activated cytoprotective program. Mitochondrial respiration and reactive oxygen species (ROS) production was measured in digitonin-permeabilized C2C12 myotubes, allowing for the modulation of mKATP conductance by changing the potassium concentration of the medium (0–130 mM). Diazoxide dose-dependently attenuated succinate-supported respiration, an effect that was independent of mKATP channel conductance. Similarly, 5-hydroxydecanoate (5-HD), a putative mKATP channel blocker, released diazoxide-induced respiratory inhibition independently of potassium concentration. Since diazoxide-induced cytoprotection and respiratory inhibition are both integrally linked to ROS generation we repeated above experiments following ROS generation using DCF fluorescence. Cytoprotective doses of diazoxide increased ROS generation independently of potassium concentration and 5-HD inhibited ROS production under the same conditions. Collectively these data support the hypothesis that diazoxide-mediated cytoprotection is independent of the conductance of the mKATP channel and rather implicate mitochondrial respiratory inhibition-triggered ROS signaling.
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      description:The ischemic preconditioning biological phenomenon has been explored to identify putative pharmacologic agents to mimic this cytoprotective program against cellular ischemic injury. Diazoxide administration confers this cytoprotection, however, whether this is via direct activation of the putative mitochondrial KATP (mKATP) channel which was originally proposed has been questioned. Here, we present data supporting an alternate hypothesis evoking mitochondrial respiratory inhibition rather than mKATP channel activation, as a mediating event in the diazoxide-activated cytoprotective program. Mitochondrial respiration and reactive oxygen species (ROS) production was measured in digitonin-permeabilized C2C12 myotubes, allowing for the modulation of mKATP conductance by changing the potassium concentration of the medium (0–130 mM). Diazoxide dose-dependently attenuated succinate-supported respiration, an effect that was independent of mKATP channel conductance. Similarly, 5-hydroxydecanoate (5-HD), a putative mKATP channel blocker, released diazoxide-induced respiratory inhibition independently of potassium concentration. Since diazoxide-induced cytoprotection and respiratory inhibition are both integrally linked to ROS generation we repeated above experiments following ROS generation using DCF fluorescence. Cytoprotective doses of diazoxide increased ROS generation independently of potassium concentration and 5-HD inhibited ROS production under the same conditions. Collectively these data support the hypothesis that diazoxide-mediated cytoprotection is independent of the conductance of the mKATP channel and rather implicate mitochondrial respiratory inhibition-triggered ROS signaling.
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