Hydroxytyrosol ameliorates oxidative stress and mitochondrial dysfunction in doxorubicin-induced cardiotoxicity in rats with breast cancer

Granados-Principal, Sergio; El-azem, Nuri; Pamplona, Reinald; Ramírez-Tortosa, César L.; Pulido-Morán, Mario; Vera-Ramírez, Laura; Quiles, José L.; Sánchez‐Rovira, Pedro; Naudí, Alba; Portero‐Otín, Manuel; Pérez-López, Patricia; Ramírez-Tortosa, M. C.

doi:10.1016/j.bcp.2014.04.001

Cited by 123 publications

(83 citation statements)

References 39 publications

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“…#P \ 0.05 significant differences compared to isoproterenol group. @P \ 0.05 significant differences compared to isoproterenol-treated group with 2 mg/kg of HT normal rats treated with HT and untreated normal group in all tested parameters such as heart weight, ratio, cardiac enzymes markers, oxidative stress statute and myocardium histology [18]. Our histopathological findings of the isoproterenol-induced myocardial infarction showed large infarcted zone with edema, necrosis and obvious separation of cardiac myofibrillar and inflammatory cells which explained the ST-segment elevation observed in the ECG findings.…”

Section: St-segment (Mv)mentioning

confidence: 92%

“…The supramaximal dose of isoproterenol also injected increased heart rate (tachycardia) due to involvement of baroreceptor reflex-mediated changes in autonomic nerve activity [17], whereas pre-and co-treatment with HT (5 mg/kg) significantly reduced the abnormalities observed in the ECG of isoproterenol-induced rats. Accordingly, it has been demonstrated that HT improved the cardiac disturbances enhanced by doxorubicin by significantly reducing the percentage of altered mitochondria also enhancing the mitochondrial electron transport chain and antioxidant defense system [18]. Several previous studies have demonstrated that the myocardium injury induced by isoproterenol in experimental rats is strongly associated with deterioration of hemodynamic and LV contractile function [14][15][16][17].…”

Section: St-segment (Mv)mentioning

confidence: 98%

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Protective Effect of Hydroxytyrosol Against Cardiac Remodeling After Isoproterenol-Induced Myocardial Infarction in Rat

Mnafgui

Hajji²,

Derbali³

et al. 2015

Cardiovasc Toxicol

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The present study aimed to investigate the cardioprotective effect of hydroxytyrosol (HT) against isoproterenol-induced myocardial infarction in rats. Male rats were randomly divided into four groups, control, isoproterenol (Isop) and pretreated animals with HT in two different doses (2 and 5 mg/kg) orally for 7 days and intoxicated with isoproterenol (Isop + HT1) and (Isop + HT2) groups. Myocardial infarction in rats was induced subcutaneously by isoproterenol (100 mg/kg, s.c.) at an interval of 24 h on 6th and 7th day. On 8th day, electrocardiographic (ECG) pattern, gravimetric and biochemical parameters were assessed. Isoproterenol exhibited changes in ECG pattern, including significant ST-segment elevation and increase in the serum troponin-T level by 317 % as compared to control rats. Moreover, cardiac injury markers (creatine kinase-MB, lactate dehydrogenase, alanine aminotransferase) underwent a notable rise in serum of infarcted animals. Else, a disturbance in lipids profile and significant increase in lipase and angiotensin-converting enzyme (ACE) activities and heart weight ratio were observed in isoproterenol group. However, pre- and co-treatment with HT (2 and 5 mg/kg) improved the myocardium injury, restored the hemodynamic function and inhibited the ACE activity that prevent cardiac hypertrophy and remodeling. Overall, these findings demonstrated that HT exerted a potent cardioprotective effect against isoproterenol-induced myocardial infarction.

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Section: St-segment (Mv)mentioning

confidence: 92%

Section: St-segment (Mv)mentioning

confidence: 98%

Protective Effect of Hydroxytyrosol Against Cardiac Remodeling After Isoproterenol-Induced Myocardial Infarction in Rat

Mnafgui

Hajji²,

Derbali³

et al. 2015

Cardiovasc Toxicol

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“…This chemical stress has been associated with the onset and development of a wide variety of diseases, such as cancer [1][2][3][4], atherosclerosis [5][6][7][8], Alzheimer's disease [9][10][11][12][13], and cardiovascular disorders [14][15][16][17][18], among many others. OS can be directly triggered by oxidative agents such as reactive oxygen species (ROS), reactive nitrogen species (RNS), and free radicals in general.…”

Section: Introductionmentioning

confidence: 99%

Free-radical scavenging by tryptophan and its metabolites through electron transfer based processes

2015

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Free-radical scavenging by tryptophan and eight of its metabolites through electron transfer was investigated in aqueous solution at physiological pH, using density functional theory and the Marcus theory. A test set of 30 free radicals was employed. Thermochemical and kinetic data on the corresponding reactions are provided here for the first time. Two different pathways were found to be the most important: sequential proton loss electron transfer (SPLET) and sequential double proton loss electron transfer (SdPLET). Based on kinetic analyses, it is predicted that the tryptophan metabolites kynurenic acid and xanthurenic acid are the best free-radical scavengers among the tested compounds; they were estimated to be at least 24 and 12 times more efficient than Trolox for scavenging (•)OOH. These findings are in line with previous reports suggesting that the antioxidant activity that has been attributed to tryptophan is actually due to its metabolites, and they demonstrate the particular importance of phenolic metabolites to such activity. Graphical Abstract Kynurenic acid (KNA) and xanthurenic acid (XNA) are the major contributors to the free-radical scavenging activity of tryptophan.

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“…Hydroxytyrosol has been shown to attenuate DOX-induced cardiotoxicity (139,140) by scavenging free radicals and protecting the respiratory chain in mitochondria (139).…”

Section: Hydroxytyrosol (29)mentioning

confidence: 99%

The Protective Role of Phenolic Compounds Against Doxorubicin-induced Cardiotoxicity: A Comprehensive Review

Razavi-Azarkhiavi

Iranshahy

Sahebkar

et al. 2016

Nutrition and Cancer

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Although doxorubicin (DOX) is among the most widely used anticancer agents, its clinical application is hampered owing to its cardiotoxicity. Adjuvant therapy with an antioxidant has been suggested as a promising strategy to reduce DOX-induced adverse effects. In this context, many phenolic compounds have been reported to protect against DOX-induced cardiotoxicity. The cardioprotective effects of phenolic compounds are exerted via multiple mechanisms including inhibition of reactive oxygen species generation, apoptosis, NF-κB, p53, mitochondrial dysfunction, and DNA damage. In this review, we present a summary of the in vitro, in vivo, and clinical findings on the protective mechanisms of phenolic compounds against DOX-induced cardiotoxicity.

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Hydroxytyrosol ameliorates oxidative stress and mitochondrial dysfunction in doxorubicin-induced cardiotoxicity in rats with breast cancer

Cited by 123 publications

References 39 publications

Protective Effect of Hydroxytyrosol Against Cardiac Remodeling After Isoproterenol-Induced Myocardial Infarction in Rat

Protective Effect of Hydroxytyrosol Against Cardiac Remodeling After Isoproterenol-Induced Myocardial Infarction in Rat

Free-radical scavenging by tryptophan and its metabolites through electron transfer based processes

The Protective Role of Phenolic Compounds Against Doxorubicin-induced Cardiotoxicity: A Comprehensive Review

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