Cisplatin-induced cardiotoxicity: Mechanisms and cardioprotective strategies

El-Awady, El-Sayed; Moustafa, Yasser M.; Abo-Elmatty, Dina M.; Radwan, Asmaa

doi:10.1016/j.ejphar.2010.09.085

Cited by 207 publications

(182 citation statements)

References 58 publications

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“…It is well known that cisplatin preferentially accumulates in the kidney, especially in the proximal tubular epithelial cells. [17][18][19][20][21][22] Our results suggest that cisplatin does not bind to liver mitochondrial GOT because cisplatin does not accumulate readily in liver tissue.…”

Section: Discussionmentioning

confidence: 75%

“…14,15) Depending on the cisplatin concentration or cellular status, tubular cell death occurs by both apoptosis and necrosis. 16) Several lines of evidence suggest that cisplatin accumulates in the mitochondria of renal cells, impairs mitochondrial bioenergetics, increases reactive oxygen species (ROS) developments, and causes the release of pro-apoptotic factors, all of which ultimately lead to renal tubular cell death, [17][18][19][20][21][22] but the mechanisms of the mitochondrial dysfunction are not yet understood. Therefore, the identification of cisplatin targets in mitochondria would be helpful to counteract cisplatininduced renal damage.…”

mentioning

confidence: 99%

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Cisplatin Binding and Inactivation of Mitochondrial Glutamate Oxaloacetate Transaminase in Cisplatin-Induced Rat Nephrotoxicity

Ozaki

Ishiguro

Itoh

et al. 2013

Bioscience, Biotechnology, and Biochemistry

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Section: Discussionmentioning

confidence: 75%

mentioning

confidence: 99%

Cisplatin Binding and Inactivation of Mitochondrial Glutamate Oxaloacetate Transaminase in Cisplatin-Induced Rat Nephrotoxicity

Ozaki

Ishiguro

Itoh

et al. 2013

Bioscience, Biotechnology, and Biochemistry

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“…According to some authors, direct myocardial toxicity may have role in the development of cisplatin-related AF [7]. El-Awady et al demonstrated that cisplatin increased serum cardiotoxicity enzymatic indices (LDH, CK and CK-MB) as well as cardiac troponin I concentration in rats compared to controls [8]. The drug is able to generate reactive oxygen species, such as superoxide anion and hydroxyl radical.…”

Section: Discussionmentioning

confidence: 99%

Recurrent Complete Atrioventricular Block During Cisplatin Infusion: A Case Report

Özcan¹,

Cirit²,

Kıykım³

2011

J Clinic Experiment Cardiol

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Cisplatin is one of the most effective chemotherapeutic agents used in the treatment of malignancies. The clinical use of cisplatin is limited by its severe adverse effects. Acute or long term cardiotoxicity is the most important doselimiting toxicity of cisplatin Cases of angina, myocardial infarction, and atrial arrhythmia have been reported during continuous infusion of cisplatin, but atrioventricular block (AV) has not been reported. Herein, we report a case with recurrent AV block that developed during cisplatin infusion, for the first time.

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“…Moreover, the heart tissue is highly perfused; therefore, exposures to the drugs occur in high concentration. Due to technical problems, we were unable to assess the oxidant status such as the status of malondialdehyde (MDA) in the heart; however, El-Awady et al (12) reported that 10 mg/ kg single dose of CIS significantly increased MDA level of heart tissue and proved that CIS is harmful to the heart tissue in animal study. Based on the tissue levels of CAT found in this study, the administration of CIS in the dose of 15 mg/kg was considered not toconsume the CAT activity of the heart tissue severely; only Troponin I level increased significantly as an early marker for cardiac injury.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Pycnogenol<sup>®</sup> on Cisplatin Induced-Cardiotoxicity in Rats

Eryılmaz¹,

Aksun²,

Demirci³

2018

meandros

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Anah tar Ke li me ler Kardiyo-onkoloji, Pycnogenol Öz AbstractObjective: This study investigated the cardiotoxicity of cisplatin (CIS) on rat heart by using the oxidative damage of the rat myocardium, Troponin I and serum S100A1 levels. Previous studies have reported that cell-protective effect of Pycnogenol® (PYC) depended on its antioxidant and anti-inflammatory properties. Hence, the myocardial protective effect of PYC was investigated in this study. Materials and Methods: Rats were randomly assigned to four groups with 5 per group. The experimental groups were as follows: Control Group, Pycnogenol Group: 10 mg/kg Pycnogenol intraperitoneally for 7 days, Cisplatin Group: 15 mg/kg single injection of cisplatin on the 5 th day intraperitoneally, Cisplatin + Pycnogenol Group: 10 mg/kg Pycnogenol for 7 days intraperitoneally, plus 15 mg/kg single injection of cisplatin on the 5 th day. The heart and serum samples were obtained on the 8 th day. Results: CIS and PYC Co-treatment group had increased catalase level (from 43.61±15.16 to 60.80±21.36, p< 0.019) and prevented Troponin I elevation (from 7.34±6.20 to 3.03±1.36). The S100A1 level was significantly reduced by CIS (from 10.25 ±8.8 to 3.99 ± 2.87, p< 0.035) and was restored by PYC treatment (32.07±29.23). Conclusion: Injured cardiomyocytes released Troponin I after exposure to CIS and PYC, which can protect the cells from CIS cardiotoxicity,increased the tissue catalase level. Additionally, PYC treatment increased serum level of S100A1.Amaç: Bu çalışma sıçan kalbi üzerinde sisplatin (CIS) kardiyotoksisitesini, sıçan miyokardı oksidatif hasarını, Troponin I ve serum S100A1 düzeylerini kullanarak araştırmıştır. Önceki çalışmalar, Pycnogenol®'in (PYC) hücre koruyucu etkisinin antioksidan ve anti-inflamatuar özelliklerine bağlı olduğunu bildirmiştir. Bu nedenle, bu çalışmada PYC'nin miyokardiyal koruyucu etkisi araştırılmıştır. Gereç ve Yöntem: Sıçanlar randomize olarak grup başına 5 olacak şekilde dört gruba ayrıldı. Kontrol grupları, pycnogenol grubu: 10 mg/kg 7 gün boyunca intraperitoneal pycnogenol, 5 gün intraperitoneal olarak sisplatin'in 15 mg/kg tek doz enjeksiyonu, Cisplatin + Pycnogenol Grubu: 10 mg/kg Pycnogenol Intraperitoneal olarak 7 gün boyunca, artı beşinci günde 15 mg/kg tek sisplatin enjeksiyonu. Kalp ve serum örnekleri 8. günde elde edildi. Bulgular: CIS ve PYC eş-tedavi grubunda katalaz seviyesi artmış (43,61±15,16'dan 60,80±21,36'ya, p<0,019) ve Troponin I yükselmesini (7,34±6,20'den 3,03±1,36'ya)

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Cisplatin-induced cardiotoxicity: Mechanisms and cardioprotective strategies

Cited by 207 publications

References 58 publications

Cisplatin Binding and Inactivation of Mitochondrial Glutamate Oxaloacetate Transaminase in Cisplatin-Induced Rat Nephrotoxicity

Cisplatin Binding and Inactivation of Mitochondrial Glutamate Oxaloacetate Transaminase in Cisplatin-Induced Rat Nephrotoxicity

Recurrent Complete Atrioventricular Block During Cisplatin Infusion: A Case Report

Protective Effect of Pycnogenol<sup>®</sup> on Cisplatin Induced-Cardiotoxicity in Rats

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