The role of peroxynitrite in chemical preconditioning with 3-nitropropionic acid in rat hearts

Turan, Nilüfer N.; Csonka, Csaba; Csont, Tamás; Giricz, Zoltán; Fodor, Gabriella; Bencsik, Péter; Gyöngyösi, Mariann; Cakici, I

doi:10.1016/j.cardiores.2005.12.012

Cited by 26 publications

(18 citation statements)

References 28 publications

(36 reference statements)

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“…Researchers also confirmed 3-NP-induced lesions and oxidative damage in hippocampus (Rodríguez-Martínez et al 2004;Silva et al 2007;Karanian et al 2006;Burda et al 2005). Turan and coworkers reported that chemical preconditioning with 3-NP reduces infarct size via a mechanism that may involve increased bioavailability of NO and decreased ONOOformation (Turan et al 2006). Previous studies from different groups reported that 3-NP significantly induced oxidative damage and impaired antioxidant defense enzymes in the brain (Kumar and Kumar 2009;Kumar et al 2006Kumar et al , 2007Túnez et al 2006Túnez et al , 2007Túnez and Santamaría 2009;Pérez-De La Cruz et al 2009;Garcia et al 2008) Antioxidant drugs strategies (Curcumin, resveratrol; Kumar et al 2006Kumar et al , 2007 as well as overexpression of genes involved in attenuating oxidative stress showed a significant neuroprotective effects against 3-NP neurotoxicity (Beal et al 1995).…”

Section: Discussionmentioning

confidence: 98%

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Kumar

2009

Psychopharmacology

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Section: Discussionmentioning

confidence: 98%

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Kumar

2009

Psychopharmacology

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“…In the Langendorff isolated and perfused heart model, the coronary vasodilator effect of Citrus paradisi peel extract could be NO-dependent since it was inhibited by NO synthase inhibition. This effect may be mediated by increased endothelial NO production, protection of superoxide-driven inactivation of NO released basally from endothelium (O 2 · − ), or potentiation of the NOcGMP pathway for the induction of relaxation (Villar et al, 2005;Turan et al, 2006).…”

Section: Discussionmentioning

confidence: 98%

Effect of Citrus paradisi extract and juice on arterial pressure both in vitro and in vivo

Díaz-Juárez

Tenorio-López

Zarco-Olvera

et al. 2009

Phytotherapy Research

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Citrus paradisi (grapefruit) consumption is considered as beneficial and it is popularly used for the treatment of a vast array of diseases, including hypertension. In the present study, the coronary vasodilator and hypotensive effects of Citrus paradisi peel extract were assessed in the Langendorff isolated and perfused heart model and in the heart and lung dog preparation. In both models, Citrus paradisi peel extract decreased coronary vascular resistance and mean arterial pressure when compared with control values (60 +/- 15 x 10(7) dyn s cm(-5) vs 100 +/- 10 x 10(7) dyn s cm(-5) and 90 mmHg vs 130 +/- 15 mmHg, respectively). These decreases in coronary vascular resistance and mean arterial pressure were blocked when isolated and perfused hearts and mongrel dogs were pre-treated with L-NAME. In humans, Citrus paradisi juice decreased diastolic arterial pressure and systolic arterial pressure both in normotensive and hypertensive subjects. Citrus paradisi juice produced a greater decrease in mean arterial pressure when compared with Citrus sinensis juice, cow milk and a vitamin C-supplemented beverage. However, more detailed studies are required to isolate, purify and evaluate the chemical compounds responsible for this pharmacological effect and to clarify its possible role for treating hypertension.

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“…ROS-induced inhibition of complex II at restoration of the coronary flow has a huge effect on subsequent mitochondrial ROS production, since it provokes its inhibition. Utilization of complex II inhibitors such as 3-nitro-N-methyl-salicylamide, malonate, or 3-nitropropionic acid indeed protects the myocardium against reperfusion-induced contractile dysfunction by reducing the burst of ROS occurring ordinarily at the beginning of reperfusion (Zhang et al 2006;Turan et al 2006;Wojtovich and Brookes 2008). In our work, ischemia/reperfusioninduced inhibition of the complex II activity in young adults related to the burst of ROS occurring at early reperfusion tempered ROS release during the remaining duration of reperfusion as it was indicated by the unchanged aconitase to fumarase ratio before and after ischemia.…”

Section: Discussionmentioning

confidence: 99%

Middle age aggravates myocardial ischemia through surprising upholding of complex II activity, oxidative stress, and reduced coronary perfusion

Mourmoura

Leguen

Dubouchaud

et al. 2010

AGE

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Aging compromises restoration of the cardiac mechanical function during reperfusion. We hypothesized that this was due to an ampler release of mitochondrial reactive oxygen species (ROS). This study aimed at characterising ex vivo the mitochondrial ROS release during reperfusion in isolated perfused hearts of middle-aged rats. Causes and consequences on myocardial function of the observed changes were then evaluated. The hearts of rats aged 10-or 52-week old were subjected to global ischemia followed by reperfusion. Mechanical function was monitored throughout the entire procedure. Activities of the respiratory chain complexes and the ratio of aconitase to fumarase activities were determined before ischemia and at the end of reperfusion. H 2 O 2 release was also evaluated in isolated mitochondria. During ischemia, middle-aged hearts displayed a delayed contracture, suggesting a maintained ATP production but also an increased metabolic proton production. Restoration of the mechanical function during reperfusion was however reduced in the middle-aged hearts, due to lower recovery of the coronary flow associated with higher mitochondrial oxidative stress indicated by the aconitase to fumarase ratio in the cardiac tissues. Surprisingly, activity of the respiratory chain complex II was better maintained in the hearts of middle-aged animals, probably because of an enhanced preservation of its membrane lipid environment. This can explain the higher mitochondrial oxidative stress observed in these conditions, since cardiac mitochondria produce much more H 2 O 2 when they oxidize FADH 2 -linked substrates than when they use NADH-linked substrates. In conclusion, the lower restoration of the cardiac mechanical activity during reperfusion in the middle-aged hearts was due to an impaired recovery of the coronary flow and an insufficient oxygen supply. The deterioration AGE (2011) of the coronary perfusion was explained by an increased mitochondrial ROS release related to the preservation of complex II activity during reperfusion.

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The role of peroxynitrite in chemical preconditioning with 3-nitropropionic acid in rat hearts

Cited by 26 publications

References 28 publications

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Effect of Citrus paradisi extract and juice on arterial pressure both in vitro and in vivo

Middle age aggravates myocardial ischemia through surprising upholding of complex II activity, oxidative stress, and reduced coronary perfusion

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