scholarly journals Effects of aging on mitochondrial hydrogen peroxide emission and calcium retention capacity in rat heart

2018 ◽  
Vol 14 (6) ◽  
pp. 920-926 ◽  
Author(s):  
Mi-Hyun No ◽  
Jun-Won Heo ◽  
Su-Zi Yoo ◽  
Han-Sam Jo ◽  
Dong-Ho Park ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Rat Heart ◽  
Retention Capacity ◽  
Calcium Retention ◽  
Effects Of Aging ◽  
Calcium Retention Capacity

scholarly journals Effect of Chronic Continuous Normobaric Hypoxia on Functional State of Cardiac Mitochondria and Tolerance of Isolated Rat Heart to Ischemia and Reperfusion: Role of µ and δ2 Opioid Receptors

2019 ◽  
pp. 909-920 ◽  
Author(s):  
E.S. Prokudina ◽  
N.V. Naryzhnaya ◽  
A.V. Mukhomedzyanov ◽  
A.S. Gorbunov ◽  
Y. Zhang ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Opioid Receptors ◽  
Mitochondrial Function ◽  
Rat Heart ◽  
Contractile Function ◽  
Isolated Rat Heart ◽  
Retention Capacity ◽  
Calcium Retention ◽  
Calcium Retention Capacity ◽  
Isolated Rat

Chronic continuous normobaric hypoxia (CNH) increases cardiac tolerance to ischemia/reperfusion injury in vivo and this effect is mediated via µ and δ2 opioid receptors (ORs) activation. CNH has also been shown to be cardioprotective in isolated rat heart. In this study, we hypothesize that this cardioprotective effect of CNH is mediated by activation of µ and δ2 ORs and preservation of mitochondrial function. Hearts from rats adapted to CNH (12 % oxygen) for 3 weeks were extracted, perfused in the Langendorff mode and subjected to 45 min of global ischemia and 30 min of reperfusion. Intervention groups were pretreated for 10 min with antagonists for different OR types: naloxone (300 nmol/l), the selective δ OR antagonist TIPP(ψ) (30 nmol/l), the selective δ1 OR antagonist BNTX (1 nmol/l), the selective δ2 OR antagonist naltriben (1 nmol/l), the selective peptide μ OR antagonist CTAP (100 nmol/l) and the selective κ OR antagonist nor-binaltorphimine (3 nmol/l). Creatine kinase activity in coronary effluent and cardiac contractile function were monitored to assess cardiac injury and functional impairment. Additionally, cardiac tissue was collected to measure ATP and to isolate mitochondria to measure respiration rate and calcium retention capacity. Adaptation to CNH decreased myocardial creatine kinase release during reperfusion and improved the postischemic recovery of contractile function. Additionally, CNH improved mitochondrial state 3 and uncoupled respiration rates, ADP/O, mitochondrial transmembrane potential and calcium retention capacity and myocardial ATP level during reperfusion compared to the normoxic group. These protective effects were completely abolished by naloxone, TIPP(ψ), naltriben, CTAP but not BNTX or nor-binaltorphimine. These results suggest that cardioprotection associated with adaptation to CNH is mediated by µ and δ2 opioid receptors activation and preservation of mitochondrial function.

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.).

scholarly journals Chloride channel blocker IAA-94 increases myocardial infarction by reducing calcium retention capacity of the cardiac mitochondria

Life Sciences ◽  
2019 ◽  
Vol 235 ◽  
pp. 116841 ◽  
Author(s):  
Devasena Ponnalagu ◽  
Ahmed Tafsirul Hussain ◽  
Rushi Thanawala ◽  
Jahnavi Meka ◽  
Piotr Bednarczyk ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Chloride Channel ◽  
Channel Blocker ◽  
Cardiac Mitochondria ◽  
Retention Capacity ◽  
Calcium Retention ◽  
Chloride Channel Blocker ◽  
Calcium Retention Capacity

scholarly journals Modification of calcium retention capacity of rat liver mitochondria by phosphate and tert-butyl hydroperoxide

2019 ◽  
pp. 59-65 ◽  
Author(s):  
R. Endlicher ◽  
Z. Drahota ◽  
Z. Červinková
Keyword(s):  
Rat Liver ◽  
Cyclosporine A ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Retention Capacity ◽  
Butyl Hydroperoxide ◽  
Calcium Retention ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide ◽  
Calcium Retention Capacity

By determining the calcium retention capacity (CRC) of rat liver mitochondria, we confirmed and extended previous observations describing the activation of mitochondrial swelling by phosphate and tert-butyl hydroperoxide (t-BHP). Using CRC measurements, we showed that both phosphate and t-BHP decrease the extent of calcium accumulation required for the full mitochondrial permeability transition pore (MPTP) opening to 35 % of control values and to only 15 % when both phosphate and t-BHP are present in the medium. When changes in fluorescence were evaluated at higher resolution, we observed that in the presence of cyclosporine A fluorescence values return after each Ca(2+) addition to basal values obtained before the Ca(2+) addition. This indicates that the MPTP remains closed. However, in the absence of cyclosporine A, the basal fluorescence after each Ca(2+) addition continuously increased. This increase was potentiated both by phosphate and t-BHP until the moment when the concentration of intramitochondrial calcium required for the full opening of the MPTP was reached. We conclude that in the absence of cyclosporine A, the MPTP is slowly opened after each Ca(2+) addition and that this rate of opening can be modified by various factors such as the composition of the media and the experimental protocol used.

scholarly journals Low-intensity treadmill exercise protects cognitive impairment by enhancing cerebellar mitochondrial calcium retention capacity in a rat model of chronic cerebral hypoperfusion

2021 ◽  
Vol 17 (5) ◽  
pp. 324-330
Author(s):  
Jae-Min Lee ◽  
Jongmin Park ◽  
Joo-Hee Lee ◽  
Hyo-Bum Kwak ◽  
Mi-Hyun No ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Treadmill Exercise ◽  
Neuroprotective Effect ◽  
Cerebral Hypoperfusion ◽  
Mitochondrial Calcium ◽  
Retention Capacity ◽  
Calcium Retention ◽  
Cerebellar Purkinje Cells ◽  
The Brain ◽  
Calcium Retention Capacity

Chronic cerebral hypoperfusion (CCH) is caused by reduced blood flow to the brain representing gradually cognitive impairment. CCH induces mitochondrial dysfunction and neuronal cell death in the brain. Exercise is known to have a neuroprotective effect on brain damage and cognitive dysfunction. This study aimed to clarify the neuroprotective effect of low-intensity treadmill exercise (LITE) by enhancing cerebellar mitochondrial calcium retention capacity in an animal model of CCH. Wistar rats were divided into the sham group, the bilateral common carotid arteries occlusion (BCCAO) group, and the BCCAO and treadmill exercise (BCCAO+Ex) group. BCCAO+Ex group engaged the LITE on a treadmill for 30 min once a day for 8 weeks before the BCCAO surgery to investigate the protective effect of LITE on cognitive impairment. CCH induced by BCCAO resulted in mitochondrial dysfunction in the cerebellum, including impaired calcium homeostasis. CCH also decreased cerebellar Purkinje cells including of calbindin D28k and parvalbumin, resulting in cognitive impairment. The impairment of mitochondrial function, loss of cerebellar Purkinje cells, and cognitive dysfunction ameliorated by exercise. The present study showed that LITE hindered the deficit of spatial working memory and loss of Purkinje cell in the cerebellum induced by CCH. We confirmed that the protective effect of LITE on Purkinje cell by enhanced the mitochondrial calcium retention capacity. We suggest that LITE may protect against cognitive impairment, and further studies are needed to develop the intervention for patients who suffered from CCH.

Sign in / Sign up

Export Citation Format

Share Document