Oxidative injury of isolated cardiomyocytes: dependence on free radical species

Durot, Isabelle; Maupoil, Véronique; Ponsard, Blandine; Cordelet, Catherine; Vergely, Catherine; Rochette, Luc; Athias, Pierre

doi:10.1016/s0891-5849(00)00382-8

Cited by 24 publications

(16 citation statements)

References 48 publications

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“…This can be reconciled with another report, showing accumulation of cellular ROS outside the cell membrane (the reasons for this are not known). 5 The major radical species detected by EPR spectroscopy in myoblast cells exposed to 2-h hypoxia were adducts of hydroxyl radicals with DMPO (four-line EPR spectrum), with a considerable contamination with another radical species (three-line spectrum), possibly a secondary oxidation product from the added DMPO (cf Fig. 3).…”

Section: Discussionmentioning

confidence: 96%

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Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury

et al. 2007

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Ischemia-reperfusion (I/R) is a condition leading to serious complications due to death of cardiac myocytes. We used the cardiomyocyte-like cell line H9c2 to study the mechanism underlying cell damage. Exposure of the cells to simulated I/R lead to their apoptosis. Over-expression of Bcl-2 and Bcl-x(L) protected the cells from apoptosis while over-expression of Bax sensitized them to programmed cell death induction. Mitochondria-targeted coenzyme Q (mitoQ) and superoxide dismutase both inhibited accumulation of reactive oxygen species (ROS) and apoptosis induction. Notably, mtDNA-deficient cells responded to I/R by decreased ROS generation and apoptosis. Using both in situ and in vivo approaches, it was found that apoptosis occurred during reperfusion following ischemia, and recovery was enhanced when hearts from mice were supplemented with mitoQ. In conclusion, I/R results in apoptosis in cultured cardiac myocytes and heart tissue largely via generation of mitochondria-derived superoxide, with ensuing apoptosis during the reperfusion phase.

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Section: Discussionmentioning

confidence: 96%

“…[3][4][5] The molecular mechanism underlying ROS generation in CMs undergoing I/R is not clear. It has been suggested that the mitochondria of stressed cells respond by generating radicals that then may result in initiating a cascade of reactions culminating in apoptosis.…”

Section: •-mentioning

confidence: 99%

Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury

et al. 2007

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“…After traumatic brain injury, the enhanced production of free radicals and other inflammatory mediators work synergistically to exacerbate injury to the brain (Tyurin et al, 2000). In cardiac injury during ischemia and reperfusion, production of free radical species is up-regulated and this damages cardiomyocytes (Durot et al, 2000). In ethanol-related liver injury, increased production of free radicals activated nuclear factor kappa B (NF-nB; Jokelainen et al, 2001).…”

Section: The Effect Of Versican On H 2 O 2 -Induced Cell Apoptosismentioning

confidence: 99%

Versican protects cells from oxidative stress-induced apoptosis

Lee

et al. 2005

Matrix Biology

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“…The production of free radicals is increased during I‐R, leading to oxidative stress‐related cellular injury through accumulation of unsaturated fatty acids in the cellular membrane. It is thought that these disorders are based on the production of various chemical mediators [9,10]. I‐R injury in the testes is a particularly serious problem because it can lead to decrease or loss of sperm stem cells, as well as infertility [3,11].…”

Section: Introductionmentioning

confidence: 99%

Protective effect of edaravone, a free‐radical scavenger, on ischaemia‐reperfusion injury in the rat testis

et al. 2010

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time simultaneously with a laser Doppler flowmeter and an NO-selective electrode, respectively. After death the tissue levels of NO 2 -NO 3 (a marker of NO production), malondialdehyde (a marker of lipid peroxidation), 8-hydroxydeoxyguanosine (a marker of oxidative DNA damage), myeloperoxidase (a marker of neutrophil infiltration), and heat-shock protein 70 (HSP 70) and its mRNA were measured. The testicular tissue was also analysed histologically. RESULTSClamping the testicular artery resulted in a decrease of blood flow to 0-5% of the basal level measured before clamping. NO release was increased during clamping and gradually recovered to the basal level on removing the clip. Interestingly, the peak of NO release in rats of the no-drug group occurred at the start of reperfusion, while that in the high-dose drug group occurred several minutes later. The levels of NO 2 -NO 3 , malondialdehyde, 8-hydroxydeoxyguanosine, myeloperoxidase and HSP 70 and its mRNA, and histological variables, were significantly greater in the no-drug I-R group than in the control, and these variables were ameliorated by treatment with edaravone. CONCLUSIONThese results indicate that edaravone reduces the oxidative stress and prevents the testicular damage induced by I-R.

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Oxidative injury of isolated cardiomyocytes: dependence on free radical species

Cited by 24 publications

References 48 publications

Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury

Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury

Versican protects cells from oxidative stress-induced apoptosis

Protective effect of edaravone, a free‐radical scavenger, on ischaemia‐reperfusion injury in the rat testis

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