Role of reactive oxygen species in cocaine-induced cardiac dysfunction

Moritz, Fabienne; Monteil, Christelle; Isabelle, Marc; Bauer, Fabrice; Renet, Sylvanie; Mulder, Paul; Richard, Vincent; Thuillez, Christian

doi:10.1016/s0008-6363(03)00499-1

Cited by 55 publications

(57 citation statements)

References 38 publications

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“…On the other hand, treatment with antioxidants could prevent cocaine-induced cardiac dysfunction. It is reported that ROS takes part in the progress of cardiomyopathy after cocaine abuse (48,49). A significant reduction was observed in SOD in opium-treated Syrian hamsters as compared to the control group.…”

Section: Superoxide Dismutase (Sod)mentioning

confidence: 90%

Study of Oxidants and Antioxidants in Addicts

Karajibani

Montazerifar

Feizabad

2016

Int J High Risk Behav Addict

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Context: This study was a systematic review that aimed to extract published articles regarding oxidant and antioxidants status in opium addiction by searching in PubMed, Google Scholar engine, SID, and Magiran databases. Evidence Acquisition: Sixty-six published articles were investigated in this review, which were selected from studies among the Iranian society and other societies from 1976 to 2015. All articles published in different fields of descriptive-analytical, experimental, and interventional studies were considered. Results: Several studies have shown that with increased production of free radicals and reactive oxygen species (ROS), the enzymatic and non-enzymatic antioxidants such as glutathione (GSH) and glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase activities, and also the concentration of vitamins A, E, C and total antioxidant capacity (TAC) decrease in opium addiction. Increased atherogenic indexes such as Low density lipoprotein/high density lipoprotein (LDL/HDL) ratio and malondialdehyde (MDA) may contribute to the increased risk of cardiovascular disease. However, it has also increased other markers of oxidative stress including: isoprostanes, 8-oxoguanine and protein carbonyl. Conclusions: Oxidative stress increases in opium-addicted people. It seems that opium is capable of provoking oxidative stress and also, has harmful effects on lipid profile and antioxidant enzyme. Drug addicts were found to have antioxidant vitamin deficiency.

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Section: Superoxide Dismutase (Sod)mentioning

confidence: 90%

Study of Oxidants and Antioxidants in Addicts

Karajibani

Montazerifar

Feizabad

2016

Int J High Risk Behav Addict

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“…Myocardial tissue MDA, a lipid peroxidation product that reacts with thiobarbituric acid, was determined as previously described [10,11]. Tissue was weighed and homogenized in a ratio of 1 g to 10 ml of 1.15% KCl.…”

Section: Myocardial Malondialdehyde (Mda) Measurementmentioning

confidence: 99%

Pyrroloquinoline Quinone (PQQ) Decreases Myocardial Infarct Size and Improves Cardiac Function in Rat Models of Ischemia and Ischemia/Reperfusion

Zhu

Zhou

Teerlink

et al. 2004

Cardiovasc Drugs Ther

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As pyrroloquinoline quinone (PQQ) is a redox cofactor in mammals, we asked if it is cardioprotective. Rats were subjected to 2 h of left anterior descending (LAD) coronary artery ligation without reperfusion (model 1, ischemia). In model 2 (ischemia/reperfusion), rats were subjected to 17 or 30 min of LAD occlusion and 2 h of reperfusion. PQQ (15-20 mg/kg) was given i.p., either 30 min before LAD occlusion (Pretreatment) or i.v. at the onset of reperfusion (Treatment). In model 1, PQQ reduced infarct size (10.0 +/- 1.5 vs 19.1 +/- 2.1%, P < 0.01). In model 2, either PQQ Pretreatment or Treatment also reduced infarct size (18.4 +/- 2.3 and 25.6 +/- 3.5% vs 38.1 +/- 2.6%, P < 0.01). PQQ resulted in higher LV developed pressure and LV (+)dP/dt after 1-2 h of reperfusion (P < 0.05), and fewer ventricular fibrillation episodes. PQQ dose (5-20 mg/kg) was inversely related to infarct size. PQQ reduced myocardial tissue levels of malondialdehyde (MDA), an indicator of lipid peroxidation (316 +/- 88 vs 99 +/- 14 nmol/g, P < 0.01). PQQ given either as Pretreatment or as Treatment at the onset of reperfusion is highly effective in reducing infarct size and improving cardiac function in a dose-related manner in rat models of ischemia and ischemia/reperfusion. The optimal dose in this study, which exhibited neither renal nor hepatic toxicity, was 15 mg/kg, but lower doses may also be efficacious. We conclude that PQQ, which appears to act as a free radical scavenger in ischemic myocardium, is a highly effective cardioprotective agent.

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“…It has been discovered recently that cocaine administration is associated with severe oxidative stress in the heart (Moritz et al, 2003;Pacifici et al, 2003;Kovacic, 2005;Ren et al, 2006;Isabelle et al, 2007). Although there are several potential enzymatic sources of ROS existing in the heart, in an animal model of chronic cocaine administration, treatment with apocynin (an NADPH oxidase inhibitor) has been reported to be effective in reducing ROS generation and to restore the cardiac output, stroke volume, and fractional shortening, suggestive of the involvement of an NADPH oxidase (Isabelle et al, 2007).…”

mentioning

confidence: 99%

Chronic Cocaine-Induced Cardiac Oxidative Stress and Mitogen-Activated Protein Kinase Activation: The Role of Nox2 Oxidase

Fan¹,

Sawbridge²,

George³

et al. 2008

J Pharmacol Exp Ther

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Chronic cocaine exposure is associated with severe cardiac complications, but the mechanisms of cocaine cardiotoxicity remain unclear, and current therapies are unsatisfactory. We investigated the hypothesis of oxidative stress-mediated cardiotoxicity and the role of NADPH oxidase in this process in a mouse model of chronic escalating "binge" cocaine administration (milligrams per kilogram): days 1 to 4 at 3 ϫ 15 mg, days 5 to 8 at 3 ϫ 20 mg, days 9 to 12 at 3 ϫ 25 mg, and days 13 to 14 at 3 ϫ 30 mg. Compared with vehicle controls, chronic binge cocaine administration significantly increased the cardiac NADPH-dependent O 2 . production (1.96-Ϯ 0.4-fold) as detected by tiron (an O 2 . scavenger)-inhibitable lucigenin chemiluminescence and dihydroethidium fluorescence. Cocaine-induced reactive oxygen species (ROS) production was associated with significant increases (ϳ2-fold) in the protein expressions of Nox2 (an isoform of NADPH oxidase) and its regulatory subunits: p22 phox

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Role of reactive oxygen species in cocaine-induced cardiac dysfunction

Abstract: These data indicate that cocaine administration induces early NADPH-driven O2-. release which may play an important role in the development and progression of the LV dysfunction observed after chronic cocaine abuse.

Cited by 55 publications

References 38 publications

Study of Oxidants and Antioxidants in Addicts

Study of Oxidants and Antioxidants in Addicts

Pyrroloquinoline Quinone (PQQ) Decreases Myocardial Infarct Size and Improves Cardiac Function in Rat Models of Ischemia and Ischemia/Reperfusion

Chronic Cocaine-Induced Cardiac Oxidative Stress and Mitogen-Activated Protein Kinase Activation: The Role of Nox2 Oxidase

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