Networking Antioxidants in the Isolated Rat Heart are Selectively Depleted by Ischemia-Reperfusion

Haramaki, Nobuya; Stewart, Daphne; Aggarwal, Sarita; Ikeda, Hisao; Reznick, Abraham Z.; Packer, Lester

doi:10.1016/s0891-5849(98)00066-5

Cited by 111 publications

(66 citation statements)

References 51 publications

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“…These alterations have also been described during ischemia and reperfusion [3,4,[31][32][33]. In this study, at the end of reperfusion after ischemic period cardiac tissue showed lesser GSH content, higher TBARS concentration and SOD cytosolic activity in comparison to non-ischemic control hearts.…”

Section: Discussionsupporting

confidence: 70%

Lipid Peroxidation and Reperfusion Injury in Hypertrophied Hearts

Fantinelli¹,

Nuñez²,

Arbeláez³

et al. 2012

Lipid Peroxidation

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Section: Discussionsupporting

confidence: 70%

Lipid Peroxidation and Reperfusion Injury in Hypertrophied Hearts

Fantinelli¹,

Nuñez²,

Arbeláez³

et al. 2012

Lipid Peroxidation

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“…Some experts have suggested that more than one antioxidant is required for clinical effectiveness settings. According to Haramaki et al 14 , the rationale is that antioxidants exist as a network wherein both lipid soluble (like tocopherals) and water soluble (ascorbate, glutathione, dihydrolipoic acid) molecules work for the removal of oxidant stress plus the regeneration of oxidant defenses. This theory reinforces the proposal of a combined scavenger therapeutic.…”

Section: Discussionmentioning

confidence: 99%

Propofol and N-Acetylcysteine attenuate oxidative stress induced by intestinal ischemia/reperfusion in rats: Protein carbonyl detection by immunoblotting

Azeredo¹,

Azeredo²,

Eleuthério³

et al. 2008

Acta Cir. Bras.

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Purpose:To evaluate the antioxidant effect of Propofol and N-Acetylcysteine (NAC) on intestinal ischemia/reperfusion (I/R) in rats by determining carbonyl protein level. Methods: Forty Wistar rats were randomly assigned into the following groups: Control; Sham; I/R with Propofol; I/R with Propofol and NAC; I/R with Ketamine and Xylazine. The I/R groups underwent 60 minutes of ischemia and an equal period of reperfusion. Blood samples, collected by cardiac punction, were centrifuged for plasma obtainment. Protein carbonyl level in plasma samples was determined by immunoblotting. Results: No significant difference in protein carbonyl level was found between Control and Sham groups (P>0.05). The highest reduction in protein carbonyl level (P<0.05) was obtained with the administration of Propofol and NAC (Group 4) in intestinal I/R procedure. Conclusion: The administration of Propofol and NAC showed the best antioxidant effect on oxidative stress in rats that underwent intestinal I/R procedure, suggesting a synergistic interaction.

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“…18,19 Many of these ROS are of mitochondrial origin, and their production increases together with the reduction of components of the respiratory chain. 20,21 This can be a result of a high membrane potential that opposes proton pumping and therefore electron transfer by respiratory chain complexes.…”

Section: Protection By Ucp1mentioning

confidence: 99%

Mitochondrial Uncoupling Protein 1 Expressed in the Heart of Transgenic Mice Protects Against Ischemic-Reperfusion Damage

et al. 2004

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Background-Mitochondrial respiration is the main source of energy in aerobic animal cells and is adapted to the energy demand by respiratory coupling. Uncoupling proteins (UCPs) perturb respiratory coupling by inducing a proton leak through the mitochondrial inner membrane. Although this could lead to deleterious energy waste, it may prevent the production of oxygen radicals when the rate of phosphorylation of ADP into ATP is low, whereas oxygen and substrate availability to mitochondria is high. The latter conditions are encountered during cardiac reperfusion after ischemia and are highly relevant to heart infarction. Methods and Results-Heart function of 6 transgenic mice expressing high amounts of UCP1 and of 6 littermate controls was compared in isolated perfused hearts in normoxia, after 40-minute global ischemia, and on reperfusion. In normoxia, oxygen consumption, contractility (quantified as the rate-pressure product), and their relationship (energetic yield) were similar in controls and transgenic mice. Although UCP1 expression did not alter the sensitivity to ischemia, it significantly improved functional recovery on reperfusion. After 60 minutes of reperfusion, contractility was 2-fold higher in transgenic mice than in controls. Oxygen consumption remained significantly depressed in controls (53Ϯ27% of control), whereas it recovered strikingly to preischemic values in transgenic mice, showing uncoupling of respiration by UCP1 activity. Glutathione and aconitase, markers of oxidative damage, indicated lower oxidative stress in transgenic mice. Conclusions-UCP1 activity is low under normoxia but is induced during ischemia-reperfusion. The presence of UCP1 mitigates reperfusion-induced damage, probably because it lowers mitochondrial hyperpolarization at reperfusion.

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Networking Antioxidants in the Isolated Rat Heart are Selectively Depleted by Ischemia-Reperfusion

Cited by 111 publications

References 51 publications

Lipid Peroxidation and Reperfusion Injury in Hypertrophied Hearts

Lipid Peroxidation and Reperfusion Injury in Hypertrophied Hearts

Propofol and N-Acetylcysteine attenuate oxidative stress induced by intestinal ischemia/reperfusion in rats: Protein carbonyl detection by immunoblotting

Mitochondrial Uncoupling Protein 1 Expressed in the Heart of Transgenic Mice Protects Against Ischemic-Reperfusion Damage

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