scholarly journals Data on effects of rotenone on calcium retention capacity, respiration and activities of respiratory chain complexes I and II in isolated rat brain mitochondria

Data in Brief ◽  
2017 ◽  
Vol 13 ◽  
pp. 707-712 ◽  
Author(s):  
Evelina Rekuviene ◽  
Laima Ivanoviene ◽  
Vilmante Borutaite ◽  
Ramune Morkuniene
Keyword(s):  
Rat Brain ◽  
Respiratory Chain ◽  
Brain Mitochondria ◽  
Respiratory Chain Complexes ◽  
Retention Capacity ◽  
Calcium Retention ◽  
Rat Brain Mitochondria ◽  
Chain Complexes ◽  
Calcium Retention Capacity ◽  
Isolated Rat

scholarly journals Characterization of Two Novel Pharmacological ATP-Sensitive Potassium Channels Modulators in Isolated Rat Heart Mitochondria

2014 ◽  
Author(s):  
Alexandra Petrus ◽  
Oana Duicu ◽  
Adrian Sturza ◽  
Lavinia Noveanu ◽  
István Baczkó ◽  
...  
Keyword(s):  
Respiratory Chain ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Heart Mitochondria ◽  
Retention Capacity ◽  
Calcium Retention ◽  
Rat Heart Mitochondria ◽  
Calcium Retention Capacity ◽  
Isolated Rat

Background Mitochondrial dysfunction plays a major role in the pathogenesis of ischemia/reperfusion injury and cardiac arrhythmias. Mitochondrial ATP-sensitive potassium channel (mitoKATP) openers such as diazoxide and pinacidil have been reported to elicit cardioprotective effects via mild uncoupling and/or respiratory chain inhibition. The aim of the present study was to characterize the effects of two novel mitoKATP modulators (KL-1488 and KL 1495) on the respiratory rates and calcium retention capacity of isolated rat heart mitochondria. Methods Mitochondrial respiratory function was assessed by high-resolution respirometry (Oxygraph-2k Oroboros Ltd.) at 370C according to the Substrate-Uncoupler-Inhibitor Titration (SUIT) protocol, as follows: complex I (CI) and complex II (CII) dependent respiration was stimulated by glutamate + malate and rotenone + succinate, respectively (State 2) and subsequent ADP (State 3, OXPHOS state) addition; cytochrome c addition evaluated the intactness of the outer mitochondrial membrane; ATP synthase was inhibited by oligomycin (State 4); uncoupled respiration was obtained by FCCP titration; respiration was inhibited with antimycin A. Calcium retention capacity (CRC) was determined by spectrofluorimetry and calculated as the amount of calcium taken by mitochondria before opening of the mitochondrial permeability transition pore (mPTP) in the presence of the pharmacological agents. Results For both C I and C II-supported respiration, 150 µM of KL 1495 (but not of KL 1488) significantly increased respiratory rates in State 2 and 4, and decreased State 3 respiration, respectively. No inhibition of mPTP opening was observed in the presence of either compound. Conclusion The mitochondrial uncoupling and respiratory chain inhibition induced by KL 1495 could play a role in cardioprotection during the postischemic reperfusion. The research was funded by the POSDRU grant no. 159/1.5/S/136893 titled “Parteneriat strategic pentru creșterea calității cercetării științifice din universitățile medicale prin acordarea de burse doctorale și postdoctorale – DocMed.Net_2.0” (A.P.).

Effects of maintenance electroshock on mitochondrial respiratory chain and creatine kinase activities in the rat brain

2012 ◽  
Vol 24 (5) ◽  
pp. 275-285
Author(s):  
Gislaine Z. Réus ◽  
Roberto B. Stringari ◽  
Gislaine T. Rezin ◽  
Daiana P. Pezente ◽  
Giselli Scaini ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Energy Metabolism ◽  
Rat Brain ◽  
Respiratory Chain ◽  
Brain Area ◽  
Mitochondrial Respiratory Chain ◽  
Respiratory Chain Complexes ◽  
Chain Complexes ◽  
Male Wistar Rats ◽  
Mitochondrial Respiratory

Réus GZ, Stringari RB, Rezin GT, Pezente DP, Scaini G, Maggi DD, De-Nês BT, Streck EL, Quevedo J, Feier G. Effects of maintenance electroshock on mitochondrial respiratory chain and creatine kinase activities in the rat brain.Objective: Electroconvulsive therapy is used efficacious treatment for a variety of complicated psychiatric disorders and evidences have indicated that energy metabolism impairment may be involved in pathophysiology and treatment of mood disorders. This work was performed to determine creatine kinase and mitochondrial respiratory chain activities at different times after the maintenance electroconvulsive shock (ECS).Methods: Male Wistar rats received a protocol mimicking therapeutic of maintenance or simulated ECS (sham) and were subsequently sacrificed immediately after, 48 h and 7 days after the last maintenance ECS. We measured creatine kinase and mitochondrial respiratory chain activities in the prefrontal cortex, hippocampus, cortex, cerebellum and striatum.Results: Our results showed that maintenance ECS alter respiratory chain complexes and creatine kinase activities in the rat brain, but these effects were related to brain area and time after the ECS, in which the animal were killed.Conclusion: Finally, these findings further support the hypothesis that alteration on the energy metabolism could be involved in the therapeutic or adverse effects of ECS.

Respiratory Activity of Isolated Rat Brain Mitochondria following in vitro Exposure to Oxygen Radicals

1983 ◽  
Vol 3 (2) ◽  
pp. 207-214 ◽  
Author(s):  
Lars Hillered ◽  
Lars Ernster
Keyword(s):  
Xanthine Oxidase ◽  
Rat Brain ◽  
Oxygen Radicals ◽  
Respiratory Activity ◽  
Brain Mitochondria ◽  
Iron Chelate ◽  
Rat Brain Mitochondria ◽  
In Vitro Exposure ◽  
Isolated Rat

Respiratory activity of isolated rat brain mitochondria was measured following in vitro exposure to oxygen radicals. The radicals were generated by hypoxanthine and xanthine oxidase in the presence of a suitable iron chelate and caused a severe inhibition of respiration stimulated by phosphate plus ADP (with malate + glutamate as substrate). The damage could be prevented by catalase or high concentrations of mannitol, but not by superoxide dismutase. A similar effect was observed when hypoxanthine and xanthine oxidase were replaced by glucose and glucose oxidase or by hydrogen peroxide. Most of the findings indicate that the hydroxyl radical is the damaging agent. It is concluded that brain mitochondria exposed to oxygen radicals in vitro show an inhibition of respiratory activity similar to that reported by other investigators as occurring in mitochondria in vivo following transient cerebral ischemia. Therefore, oxygen radicals may contribute to this type of cell damage.

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