Effect of NaHS, Hydrogen Sulfide Donor, on the Functional State of the Respiratory Chain in the Rat Heart Mitochondria

2014 ◽  
Vol 5 (2) ◽  
pp. 159-170
Author(s):  
Olena M. Semenykhina ◽  
Nataliya A. Strutynska ◽  
Alina Yu. Budko ◽  
Galyna L. Vavilova ◽  
Vadim F. Sagach
Keyword(s):  
Hydrogen Sulfide ◽  
Respiratory Chain ◽  
Functional State ◽  
Rat Heart ◽  
Heart Mitochondria ◽  
Rat Heart Mitochondria

scholarly journals Effect of hydrogen sulfide donor NaHs on the functional state of the respiratory chain of the rat heart mitochondria

2013 ◽  
Vol 59 (2) ◽  
pp. 9-17 ◽  
Author(s):  
OM Semenykhina ◽  
◽  
NA Strutyns'ka ◽  
AIu Bud'ko ◽  
HL Vavilova ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Respiratory Chain ◽  
Functional State ◽  
Rat Heart ◽  
Heart Mitochondria ◽  
Rat Heart Mitochondria

scholarly journals The effect of respiratory chain impairment of β-oxidation in rat heart mitochondria

1996 ◽  
Vol 319 (2) ◽  
pp. 633-640 ◽  
Author(s):  
Simon EATON ◽  
Morteza POURFARZAM ◽  
Kim BARTLETT
Keyword(s):  
Respiratory Chain ◽  
Rat Heart ◽  
Redox State ◽  
Complex Iii ◽  
Heart Mitochondria ◽  
Cardiac Ischaemia ◽  
Low Concentrations ◽  
Rat Heart Mitochondria ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
14Co2 Release

Cardiac ischaemia leads to an inhibition of β-oxidation flux and an accumulation of acyl-CoA and acyl-carnitine esters in the myocardium. However, there remains some uncertainty as to which esters accumulate during cardiac ischaemia and therefore the site of inhibition of β-oxidation [Moore, Radloff, Hull and Sweely (1980) Am. J. Physiol. 239, H257-H265; Latipää (1989) J. Mol. Cell. Cardiol. 21, 765–771]. When β-oxidation of hexadecanoyl-CoA in state III rat heart mitochondria was inhibited by titration of complex III activity, flux measured as 14CO2 release, acid-soluble radioactivity or as acetyl-carnitine was progressively decreased. Low concentrations of myxothiazol caused reduction of the ubiquinone pool whereas the NAD+/NADH redox state was less responsive. Measurement of the CoA and carnitine esters generated under these conditions showed that there was a progressive decrease in the amounts of chain-shortened saturated acyl esters with increasing amounts of myxothiazol. The concentrations of 3-hydroxyacyl and 2-enoyl esters, however, were increased between 0 and 0.2 µM myxothiazol but were lowered at higher myxothiazol concentrations. More hexadecanoyl-CoA and hexadecanoyl-carnitine were present with increasing concentrations of myxothiazol. We conclude that 3-hydroxyacyl-CoA dehydrogenase and acyl-CoA dehydrogenase activities are inhibited by reduction of the ubiquinone pool, and that this explains the confusion over which esters of CoA and carnitine accumulate during cardiac ischaemia. Furthermore these studies demonstrate that the site of the control exerted by the respiratory chain over β-oxidation is shifted depending on the extent of the inhibition of the respiratory chain.

scholarly journals The Identification of Prohibitin in the Rat Heart Mitochondria in Heart Failure

Biomedicines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1793
Author(s):  
Yulia Baburina ◽  
Roman Krestinin ◽  
Irina Odinokova ◽  
Irina Fadeeva ◽  
Linda Sotnikova ◽  
...  
Keyword(s):  
Heart Failure ◽  
Respiratory Chain ◽  
Rat Heart ◽  
Heart Function ◽  
Protective Action ◽  
Heart Mitochondria ◽  
Supramolecular Organization ◽  
Experimental Conditions ◽  
Mitochondria Of The Heart ◽  
Rat Heart Mitochondria

Mitochondria are considered the main organelles in the cell. They play an important role in both normal and abnormal heart function. There is a supramolecular organization between the complexes of the respiratory chain (supercomplexes (SCs)), which are involved in mitochondrial respiration. Prohibitins (PHBs) participate in the regulation of oxidative phosphorylation (OXPHOS) activity and interact with some subunits of the OXPHOS complexes. In this study, we identified a protein whose level was decreased in the mitochondria of the heart in rats with heart failure. This protein was PHB. Isoproterenol (ISO) has been used as a compound to induce heart failure in rats. We observed that astaxanthin (AX) increased the content of PHB in rat heart mitochondria isolated from ISO-injected rats. Since it is known that PHB forms complexes with some mitochondrial proteins and proteins that are part of the complexes of the respiratory chain, the change in the levels of these proteins was investigated under our experimental conditions. We hypothesized that PHB may be a target for the protective action of AX.

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.).

Magnolol and honokiol isolated from magnolia officinalis protect rat heart mitochondria against lipid peroxidation

1994 ◽  
Vol 47 (3) ◽  
pp. 549-553 ◽  
Author(s):  
Yu-Chiang Lo ◽  
Teng Che-Ming ◽  
Chen Chieh-Fu ◽  
Chen Chien-Chih ◽  
Hong Chuang-Ye
Keyword(s):  
Lipid Peroxidation ◽  
Rat Heart ◽  
Heart Mitochondria ◽  
Rat Heart Mitochondria ◽  
Magnolia Officinalis

Involvement of SH-groups during interaction of diazoxide with the inner membrane of rat heart mitochondria

2007 ◽  
Vol 415 (1) ◽  
pp. 206-210 ◽  
Author(s):  
S. M. Korotkov ◽  
V. P. Nesterov ◽  
L. V. Emel’yanova ◽  
N. N. Ryabchikov
Keyword(s):  
Rat Heart ◽  
Heart Mitochondria ◽  
Inner Membrane ◽  
Sh Groups ◽  
Rat Heart Mitochondria

Abstract 104: Effects of Pinacidil and Ca 2 + on Sodium-loaded Rat Heart Mitochondria

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Sergey M Korotkov ◽  
Vladimir P Nesterov ◽  
Irina V Brailovskaya ◽  
Larisa V Emelyanova ◽  
Svetlana A Konovalova ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Rat Heart ◽  
Mitochondrial Membrane ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion ◽  
Potassium Acetate ◽  
Heart Mitochondria ◽  
Inner Mitochondrial Membrane ◽  
Rat Heart Mitochondria ◽  
Acetate Medium

Deterioration of the contractile parameters of the heart muscle caused by ischemia and followed reperfusion is known as the main postoperative complication which is related to Ca 2+ and Na + overload in cardiomyocytes and mitochondria. Pinacidil reduced the overload in ischemia/reperfusion experiments. The mechanism of this phenomenon is still not clear. We hypothesized that increased ion permeability of the inner mitochondrial membrane (IMM) followed drop of electrochemical potential (ΔΨ mito ) can reduce the calcium. The aim of the study was to elucidate the effect of pinacidil (100 μM) and Ca 2+ (100 μM ) on swelling, oxygen consumption and ΔΨ mito of isolated sodium-loaded rat heart mitochondria (RHM(Na)) energized glutamate and malate. Pinacidil significantly enchanced the permeability of IMM to protons in ammonium nitrate medium. Also increased swelling of RHM(Na) energized with substrates in potassium acetate medium revealed that pinacidil increased potassium transport into matrix. Pinacidil stimulated oxygen consumption of RHM(Na) in State 4 and detained Ca 2+ -induced dissipation of ΔΨ mito . Under condition of Ca 2+ and Na + overload simulating ischemia/reperfusion, RHM(Na) oxygen consumption was not affected with pinacidil in State 3 and in the presence of 2,4-dinitrophenol. Cyclosporin A and ADP, the inhibitors of mitochondrial permeability transition pore (MPTP), markedly decreased Ca 2+ - induced swelling of RHM(Na) in nitrate ammonium or potassium acetate medium in the presence of pinacidil. Carboxyatractyloside, an inhibitor of cytosolic side-specific adenine nucleotide translocase, eliminated a pinacidil-stimulated oxygen consumption of succinate-energized RHMNa in State 4 regardless of the presence of Ca 2+ . Pinacidil was also concluded to accelerat potassium flux into energized RHM(Na) and promot MPTP opening in the low conduction state. Based on our data we suggested that the effect of pharmacological preconditioning induced by pinacidil could be due to it’s direct effect on mitochondria which is connected with above stimulation of the potassium permeability of the inner mitochondrial membrane and following reduce of the ΔΨ mito that thus prevent calcium overload of cardiomyocytes after ischemia/reperfusion in turn.

Structure of paracrystalline arrays on outer membranes of rat-liver and rat-heart mitochondria

1992 ◽  
Vol 108 (3) ◽  
pp. 227-237 ◽  
Author(s):  
C.A. Mannella ◽  
A. Ribeiro ◽  
B. Cognon ◽  
D. D'Arcangelis
Keyword(s):  
Rat Liver ◽  
Rat Heart ◽  
Heart Mitochondria ◽  
Outer Membranes ◽  
Rat Heart Mitochondria
Sign in / Sign up

Export Citation Format

Share Document