Impairment of mitochondrial respiratory activity in the early ischemic myocardium. With special reference to electron transport system.

Geshi, Eiichi; Konno, Noburu; Yanagishita, Toshikuni; Kubo, Takashi

doi:10.1253/jcj.52.535

Cited by 21 publications

(10 citation statements)

References 27 publications

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“…This conclusion was supported by studies demonstrating that, during relatively short periods of ischaemia (20-30 min), complex I activity gradually decreases in parallel with the decrease in mitochondrial respiration with NAD + -dependent respiration [48,50]. The activity of complex III was found also to decrease, but more gradually, and that of complex V decreased most rapidly (by 40% after 5 min of global ischaemia), whereas the activities of complexes II and IV were unchanged [50,51]. Total ligation of the dog heart left anterior descending coronary artery for 30 min and 60 min decreased the state 3 respiration rate (~80%) and complex I activity (~70%), and these did not recover on reperfusion [51].…”

Section: Which Components Of Oxidative Phosphorylation Are Affected Bmentioning

confidence: 80%

In the eye of the storm: mitochondrial damage during heart and brain ischaemia

2013

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We review research investigating mitochondrial damage during heart and brain ischaemia, focusing on the mechanisms and consequences of ischaemia-induced and/or reperfusion-induced: (a) inhibition of mitochondrial respiratory complex I; (b) release of cytochrome c from mitochondria; (c) changes to mitochondrial phospholipids; and (d) nitric oxide inhibition of mitochondria. Heart ischaemia causes inhibition of cytochrome oxidase and complex I, release of cytochrome c, and induction of permeability transition and hydrolysis and oxidation of mitochondrial phospholipids, but some of the mechanisms are unclear. Brain ischaemia causes inhibition of complexes I and IV, but other effects are less clear.

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Section: Which Components Of Oxidative Phosphorylation Are Affected Bmentioning

confidence: 80%

In the eye of the storm: mitochondrial damage during heart and brain ischaemia

2013

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“…Some investigators have reported a defect at the level of the electron transport chain (20), whereas others have indicated that changes in mitochondrial membrane potentials (5) and mitochondrial permeability (11) may induce the I/R-induced changes in mitochondrial function. Lipid peroxidation of mitochondrial membrane (32) and a decrease in cardiolipin content (27,31) as a consequence of oxidative stress have also been shown to serve as mechanisms for changes in mitochondrial respiration and oxidative phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

Role of oxidative stress in alterations of mitochondrial function in ischemic-reperfused hearts

Makazan¹,

Saini²,

Dhalla³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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Makazan Z, Saini HK, Dhalla NS. Role of oxidative stress in alterations of mitochondrial function in ischemic-reperfused hearts. Am J Physiol Heart Circ Physiol 292: H1986 -H1994, 2007. First published December 15, 2006; doi:10.1152/ajpheart.01214.2006.-To study the mechanisms of mitochondrial dysfunction due to ischemiareperfusion (I/R) injury, rat hearts were subjected to 20 or 30 min of global ischemia followed by 30 min of reperfusion. After recording both left ventricular developed pressure (LVDP) and end-diastolic pressure (LVEDP) to monitor the status of cardiac performance, mitochondria from these hearts were isolated to determine respiratory and oxidative phosphorylation activities. Although hearts subjected to 20 min of ischemia failed to generate LVDP and showed a marked increase in LVEDP, no changes in mitochondrial respiration and phosphorylation were observed. Reperfusion of 20-min ischemic hearts depressed mitochondrial function significantly but recovered LVDP completely and lowered the elevated LVEDP. On the other hand, depressed LVDP and elevated LVEDP in 30-min ischemic hearts were associated with depressions in both mitochondrial respiration and oxidative phosphorylation. Reperfusion of 30-min ischemic hearts elevated LVEDP, attenuated LVDP, and decreased mitochondrial state 3 and uncoupled respiration, respiratory control index, ADP-to-O ratio, as well as oxidative phosphorylation rate. Alterations of cardiac performance and mitochondrial function in I/R hearts were attenuated or prevented by pretreatment with oxyradical scavenging mixture (superoxide dismutase and catalase) or antioxidants [N-acetyl-L-cysteine or N-(2-mercaptopropionyl)-glycine]. Furthermore, alterations in cardiac performance and mitochondrial function due to I/R were simulated by an oxyradical-generating system (xanthine plus xanthine oxidase) and an oxidant (H 2O2) either upon perfusing the heart or upon incubation with mitochondria. These results support the view that oxidative stress plays an important role in inducing changes in cardiac performance and mitochondrial function due to I/R. cardiac performance; oxidative phosphorylation; mitochondrial respiration; oxyradicals; antioxidants BY VIRTUE OF THEIR ABILITY to carry on the processes of oxidative phosphorylation and electron transport, mitochondria are the major source of energy production in the form of ATP, which is required for cardiac contraction and relaxation (19,26,46). Mitochondria are also known to accumulate a substantial amount of Ca 2ϩ and are considered to serve as a sink to maintain the intracellular concentration of free Ca 2ϩ within certain limits (18,19,26). However, an excessive amount of intracellular Ca 2ϩ results in the overloading of mitochondria with Ca 2ϩ

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“…Such transmural differences are well known but, whether they are associated with transmural differences in mitochondrial complex activities deserves further analysis. Indeed, differences in subendo- and Epi mitochondria or their regulation were expected but, previous reports showed no or minor differences when considering metabolic enzymes or electron transport system (Geshi et al, 1988; Gallego-Delgado et al, 2006). However, there are few data comparing endo- and epicardium layers mitochondrial function in the normal LV, especially using saponin-skinned fibers that ensure global mitochondrial function assessment in intact mitochondria (MacDonald et al, 2011).…”

Section: Introductionmentioning

confidence: 94%

Pressure overload-induced mild cardiac hypertrophy reduces left ventricular transmural differences in mitochondrial respiratory chain activity and increases oxidative stress

Kindo¹,

Gerelli²,

Bouitbir³

et al. 2012

Front. Physio.

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Objective: Increased mechanical stress and contractility characterizes normal left ventricular (LV) subendocardium (Endo) but whether Endo mitochondrial respiratory chain complex activities is reduced as compared to subepicardium (Epi) and whether pressure overload-induced LV hypertrophy (LVH) might modulate transmural gradients through increased reactive oxygen species (ROS) production is unknown. Methods: LVH was induced by 6 weeks abdominal aortic banding and cardiac structure and function were determined with echocardiography and catheterization in sham-operated and LVH rats (n = 10 for each group). Mitochondrial respiration rates, coupling, content and ROS production were measured in LV Endo and Epi, using saponin-permeabilized fibers, Amplex Red fluorescence and citrate synthase activity. Results: In sham, a transmural respiratory gradient was observed with decreases in endo maximal oxidative capacity (−36.7%, P < 0.01) and complex IV activity (−57.4%, P < 0.05). Mitochondrial hydrogen peroxide (H2O2) production was similar in both LV layers. Aortic banding induced mild LVH (+31.7% LV mass), associated with normal LV fractional shortening and end diastolic pressure. LVH reduced maximal oxidative capacity (−23.6 and −33.3%), increased mitochondrial H2O2 production (+86.9 and +73.1%), free radical leak (+27.2% and +36.3%) and citrate synthase activity (+27.2% and +36.3%) in Endo and Epi, respectively. Transmural mitochondrial respiratory chain complex IV activity was reduced in LVH (−57.4 vs. −12.2%; P = 0.02). Conclusions: Endo mitochondrial respiratory chain complexes activities are reduced compared to LV Epi. Mild LVH impairs mitochondrial oxidative capacity, increases oxidative stress and reduces transmural complex IV activity. Further studies will be helpful to determine whether reduced LV transmural gradient in mitochondrial respiration might be a new marker of a transition from uncomplicated toward complicated LVH.

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Impairment of mitochondrial respiratory activity in the early ischemic myocardium. With special reference to electron transport system.

Cited by 21 publications

References 27 publications

In the eye of the storm: mitochondrial damage during heart and brain ischaemia

In the eye of the storm: mitochondrial damage during heart and brain ischaemia

Role of oxidative stress in alterations of mitochondrial function in ischemic-reperfused hearts

Pressure overload-induced mild cardiac hypertrophy reduces left ventricular transmural differences in mitochondrial respiratory chain activity and increases oxidative stress

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