Right and Left Myocardial Antioxidant Responses During Heart Failure Subsequent to Myocardial Infarction

Hill, Michael; Singal, Pawan K.

doi:10.1161/01.cir.96.7.2414

Cited by 371 publications

(349 citation statements)

References 39 publications

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“…33,34 Thus, our findings of an association between increased GGT activity and depressed LV systolic function supports the importance of oxidative stress in CAD.…”

Section: Relation Of Ggt Activity With Inflammation and LV Functionsupporting

confidence: 80%

The Importance of Gamma‐Glutamyltransferase Activity in Patients with Coronary Artery Disease

Demircan

Yazıcı

Durna

et al. 2009

Clinical Cardiology

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Background: In this study, we sought to investigate the relation of gamma-glutamyltransferase (GGT) levels with the significance of coronary artery disease (CAD), clinical presentation, left ventricular (LV) function, and inflammatory activity. Methods: A total of 235 patients (mean age: 60.1 ± 10.5 years, 166 [70%] males) who had coronary angiography were included in the study. Patients who had CAD constituted the study group (Group 1, n = 189) and patients who had insignificant coronary disease or normal coronary activity constituted the control group (Group 2, n = 46). Results: GGT levels were higher in Group 1 than Group 2 (38.7 ± 30.9 U/L versus 27.5 ± 17.5 U/L, p = 0.025). Left ventricular ejection fraction (LVEF) was lower in Group 1 than Group 2 (52.6%±11.7% versus 58.8%±11.3%, p<0.002). GGT activity (40.2 ± 32.5 U/L versus 29.1 ± 18.3 U/L, p<0.002) and c-reactive protein (CRP) levels (33.9 ± 43.6 mg/dl versus 17.8 ± 29.8 mg/dl, p<0.002) were higher, LVEF (52.6%±12.1% versus 56.5%±11.0%, p = 0.021) was lower in patients with acute coronary syndrome compared with stable CAD group. In regression analysis, CRP levels (p<0.0001, odds ratio [OR] = 3.77, 95% confidence interval [CI] 0.10

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“…33,34 Thus, our findings of an association between increased GGT activity and depressed LV systolic function supports the importance of oxidative stress in CAD.…”

Section: Relation Of Ggt Activity With Inflammation and LV Functionsupporting

confidence: 80%

The Importance of Gamma‐Glutamyltransferase Activity in Patients with Coronary Artery Disease

Demircan

Yazıcı

Durna

et al. 2009

Clinical Cardiology

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“…In Fact, at physiological levels, ROS are involved in cellular signaling and maintain homeostasis (26) but excessive ROS cause , protein oxidation lipid peroxidation, and DNA damage .These events could lead to irreversible cell damage and death, which have been implicated in a wide range of pathological cardiovascular conditions (27)(28)(29).…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

Koohsari

Shaki

Jahani

2016

Braz. arch. biol. technol.

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Methamphetamine (METH) is widely abused in worldwide. METH use could damage the dopaminergic system and induce cardiotoxicity via oxidative stress and mitochondrial dysfunction. Edaravone, a sedative-hypnotic agent, is known for it's antioxidant properties. In this study we used edaravone for attenuating of METH-induced cardiotoxicity in rats. The groups (six rats in each group) were as follows: control, METH (5 mg/kg IP) and edaravone (5, 10 and 20 mg/kg, IP) was administered 30 min before METH. After 24 hours, animals were killed, heart tissue was separated and mitochondrial fraction was isolated and oxidative stress markers were measured. Edaravone significantly (p<0.05) protected the heart against lipid peroxidation by inhibition of reactive oxygen species (ROS) formation. Edaravone also significantly (p<0.05) increased the levels of heart glutathione (GSH). METH administration significantly (p<0.05) disrupted mitochondrial function that edaravone pre-treatment significantly (p<0.05) inhibited METHinduced mitochondrial dysfunction. Protein carbonyl level also increased after METH exposure, but was significantly (p<0.05) decreased with edaravone pre-treatment. These results suggested that edaravone is able to inhibition of METH-induced oxidative stress and mitochondrial dysfunction and subsequently METH-induced cardiotoxicity. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH toxicity and cardio degenerative disease.

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“…Previous studies have pointed out changes in the redox status of glutathione in the failing heart [20], but have overlooked a possible deficiency in glutathione content.…”

Section: Discussionmentioning

confidence: 99%

“…Of note, the well-being of the patients affected with those diseases is improved by treatment with the glutathione precursor N-acetylcysteine (NAC) [13,14,18,19]. Previous studies pointed out the decrease in cardiac GSH/ GSSG ratio in CHF [20,21]. However, the possible deficiency in total glutathione in the failing heart, and its related possible metabolic consequences have been overlooked.…”

Section: Introductionmentioning

confidence: 99%

Neutral sphingomyelinase inhibition participates to the benefits of N-acetylcysteine treatment in post-myocardial infarction failing heart rats

Adamy

Mulder

Khouzami

et al. 2007

Journal of Molecular and Cellular Cardiology

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Deficiency in cellular thiol tripeptide glutathione (L-γ glutamyl-cysteinyl-glycine) determines the severity of several chronic and inflammatory human diseases that may be relieved by oral treatment with the glutathione precursor N-acetylcysteine (NAC).Here, we showed that the left ventricle (LV) of human failing heart was depleted in total glutathione by 54%. Similarly, 2-month post-myocardial infarction (MI) rats, with established chronic heart failure (CHF), displayed deficiency in LV glutathione. Onemonth oral NAC treatment normalized LV glutathione, improved LV contractile function and lessened adverse LV remodelling in 3-month post-MI rats. Biochemical studies at two time-points of NAC treatment, 3 days and 1 month, showed that inhibition of the neutral sphingomyelinase (N-SMase), Bcl-2 depletion and caspase-3 activation, were key, early and lasting events associated with glutathione repletion. Attenuation of oxidative stress, downregulation of the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) and its TNF-R1 receptor were significant after 1-month NAC treatment. These data indicate that, besides glutathione deficiency, N-SMase activation is associated with post-MI CHF progression, and that blockade of N-SMase activation participates to post-infarction failing heart recovery achieved by NAC treatment. NAC treatment in post-MI rats is a way to disrupt the vicious sTNF-α/ TNF-R1/ N-SMase cycle.

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Right and Left Myocardial Antioxidant Responses During Heart Failure Subsequent to Myocardial Infarction

Cited by 371 publications

References 39 publications

The Importance of Gamma‐Glutamyltransferase Activity in Patients with Coronary Artery Disease

The Importance of Gamma‐Glutamyltransferase Activity in Patients with Coronary Artery Disease

Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

Neutral sphingomyelinase inhibition participates to the benefits of N-acetylcysteine treatment in post-myocardial infarction failing heart rats

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