Mitochondrial toxicity of cardiac drugs and its relevance to mitochondrial disorders

Finsterer, Josef; Zarrouk‐Mahjoub, Sinda

doi:10.1517/17425255.2015.973401

Cited by 22 publications

(17 citation statements)

References 56 publications

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“…Propranolol and atenolol at 5, 10 and 20 µg/ml increased ROS generation in the mitochondria obtained from the heart. These results are in agreement with previous studies which showed some beta-blockers can increase the generation of ROS in several tissues [7,8]. Thus, propranolol and atenolol may impair cardiac function through increase the generation of ROS.…”

Section: Discussionsupporting

confidence: 93%

“…Propranolol (nonselective β receptor blocker) and atenolol (β 1 selective Beta-blockers) are among the beta-blocker drugs used in the treatment of many CVDs [4][5][6]. It has been shown that mitochondria are one of the targets of cardiac drugs, and also most of these drugs can cause mitochondrial toxicity [7]. Research has shown that some beta-blocker drugs are able to a generation of reactive oxygen species (ROS) [7,8].…”

Section: Introductionmentioning

confidence: 99%

“…It has been shown that mitochondria are one of the targets of cardiac drugs, and also most of these drugs can cause mitochondrial toxicity [7]. Research has shown that some beta-blocker drugs are able to a generation of reactive oxygen species (ROS) [7,8]. Furthermore, some beta-blockers (such as propranolol) cause alterations in mitochondrial membrane and morphology, mitochondrial swelling, cytochrome c release, and induction of caspase cascade and cell death (apoptosis) [9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

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Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

2020

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Propranolol and atenolol are known as β receptor blocker drugs. These drugs are used to treat some heart diseases. There are controversies in the relationship between the use of beta-blocker drugs and the level of reactive oxygen species (ROS). Mitochondria as one of the most important sources of ROS are considered as one of the targets of drug-induced cardiotoxicity. The aim of this study was to evaluate the effects of propranolol and atenolol on mitochondria isolated from the heart. To achieve this aim, several markers of mitochondrial and cellular toxicity were evaluated. The key results of this study are the increased ROS level, collapse in mitochondrial membrane potential (MMP), mitochondrial swelling and cytochrome c release as well as disruption of respiratory chain complex II in mitochondria in isolated heart mitochondria after exposure to propranolol and atenolol. The results indicate an increase in caspase-3 activity and a decrease in the ATP level in cardiomyocytes after exposure to propranolol and atenolol. The underlying mechanisms of propranolol and atenolol induced cardiotoxicity may be associated with alterations in mitochondrial function, oxidative stress, and changes in the mitochondrial membrane.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

2020

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“…Leukopenia, in addition to toxic neurological effects, is the primary toxic effect of DTX [ 47 ]. But, in human neutrophils, granulocytes, and lymphocytes, clopidogrel has been shown to decrease the membrane potential of the inner mitochondrial membrane, increase ROS production, and induce cytochrome-c release into the cytoplasm ultimately leading to apoptosis [ 55 ]. Therefore, leukocytes affected by anticancer drugs may be more susceptible to apoptotic process during combined treatment with clopidogrel.…”

Section: Discussionmentioning

confidence: 99%

Clopidogrel in a combined therapy with anticancer drugs—effect on tumor growth, metastasis, and treatment toxicity: Studies in animal models

et al. 2017

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Clopidogrel, a thienopyridine derivative with antiplatelet activity, is widely prescribed for patients with cardiovascular diseases. In addition to antiplatelet activity, antiplatelet agents possess anticancer and antimetastatic properties. Contrary to this, results of some studies have suggested that the use of clopidogrel and other thienopyridines accelerates the progression of breast, colorectal, and prostate cancer. Therefore, in this study, we aimed to evaluate the efficacy of clopidogrel and various anticancer agents as a combined treatment using mouse models of breast, colorectal, and prostate cancer. Metastatic dissemination, selected parameters of platelet morphology and biochemistry, as well as angiogenesis were assessed. In addition, body weight, blood morphology, and biochemistry were evaluated to test toxicity of the studied compounds. According to the results, clopidogrel increased antitumor and/or antimetastatic activity of chemotherapeutics such as 5-fluorouracil, cyclophosphamide, and mitoxantrone, whereas it decreased the anticancer activity of doxorubicin, cisplatin, and tamoxifen. The mechanisms of such divergent activities may be based on the modulation of tumor vasculature via factors, such as transforming growth factor β1 released from platelets. Moreover, clopidogrel increased the toxicity of docetaxel and protected against mitoxantrone-induced toxicity, which may be due to the modulation of hepatic enzymes and protection of the vasculature, respectively. These results demonstrate that antiplatelet agents can be useful but also dangerous in anticancer treatment and therefore use of thienopyridines in patients undergoing chemotherapy should be carefully evaluated.

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“…LD triggers apoptosis in several cellular models by impairment of respiratory chain functions resulting in reduced ATP production, depolarization of the mitochondria, loss of mitochondrial membrane potential ( ∆ Ψ), and overproduction of intracellular ROS [ 10 , 17 , 29 – 34 ]. The increased production of ROS correlates with decreased cell viability after exposure to LD, and ROS plays a vital role in inducing apoptosis of corneal cells and corneal endothelial dysfunction [ 34 – 37 ].…”

Section: Discussionmentioning

confidence: 99%

Sodium Ferulate Attenuates Lidocaine‐Induced Corneal Endothelial Impairment

Jiang

Fan

2018

Oxidative Medicine and Cellular Longevity

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The introduction of intracameral anaesthesia by injection of lidocaine has become popular in cataract surgery for its inherent potency, rapid onset, tissue penetration, and efficiency. However, intracameral lidocaine causes corneal thickening, opacification, and corneal endothelial cell loss. Herein, we investigated the effects of lidocaine combined with sodium ferulate, an antioxidant with antiapoptotic and anti-inflammatory properties, on lidocaine-induced damage of corneal endothelia with in vitro experiment of morphological changes and cell viability of cultured human corneal endothelial cells and in vivo investigation of corneal endothelial cell density and central corneal thickness of cat eyes. Our finding indicates that sodium ferulate from 25 to 200 mg/L significantly reduced 2 g/L lidocaine-induced toxicity to human corneal endothelial cells, and 50 mg/L sodium ferulate recovered the damaged human corneal endothelial cells to normal growth status. Furthermore, 100 mg/L sodium ferulate significantly inhibited lidocaine-induced corneal endothelial cell loss and corneal thickening in cat eyes. In conclusion, sodium ferulate protects human corneal endothelial cells from lidocaine-induced cytotoxicity and attenuates corneal endothelial cell loss and central corneal thickening of cat eyes after intracameral injection with lidocaine. It is likely that the antioxidant effect of sodium ferulate reduces the cytotoxic and inflammatory corneal reaction during intracameral anaesthesia.

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Mitochondrial toxicity of cardiac drugs and its relevance to mitochondrial disorders

Cited by 22 publications

References 56 publications

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

Clopidogrel in a combined therapy with anticancer drugs—effect on tumor growth, metastasis, and treatment toxicity: Studies in animal models

Sodium Ferulate Attenuates Lidocaine‐Induced Corneal Endothelial Impairment

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