Cardiotoxicity of copper-based antineoplastic drugs casiopeinas is related to inhibition of energy metabolism

Hernández‐Esquivel, Luz; Marín‐Hernández, Álvaro; Pavón, Natalia; Carvajal, Karla; Moreno‐Sánchez, Rafael

doi:10.1016/j.taap.2005.06.023

Cited by 56 publications

(30 citation statements)

References 26 publications

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“…The most evaluated cardiac toxicity is that produced by anthracyclines (Hirano et al, 1993; Soga et al, 2006; Berdichevski et al, 2010; Shaker and Sourour, 2010). However, this cardiotoxicity is not unique to this group of antineoplastic drugs, but may occur with other antitumoral agent groups (Al-Majed et al, 2006; Drimal et al, 2006; Hernández-Esquivel et al, 2006; Sudharsan et al, 2006), including cisplatin (Pai and Nahata, 2000). It was reported that treatment with a single dose of cisplatin causes left ventricular dysfunction and depression of cardiomyocyte contractility in the rat.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Cardiovascular Alterations Induced by Different Chronic Cisplatin Treatments

et al. 2017

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In the last years, many clinical studies have revealed that some cisplatin-treated cancer survivors have a significantly increased risk of cardiovascular events, being cisplatin-induced cardiovascular toxicity an increasing concern. The aim of the present work was to evaluate the cardiovascular alterations induced by different chronic cisplatin treatments, and to identify some of the mechanisms involved. Direct blood pressure, basal cardiac (left ventricle and coronary arteries) and vascular (aortic and mesenteric) functions were evaluated in chronic (5 weeks) saline- or cisplatin-treated male Wistar rats. Three different doses of cisplatin were tested (1, 2, and 3 mg/kg/week). Alterations in cardiac and vascular tissues were also investigated by immunohistochemistry, Western Blot, and or quantitative RT-PCR analysis. Cisplatin treatment provoked a significant modification of arterial blood pressure, heart rate, and basal cardiac function at the maximum dose tested. However, vascular endothelial dysfunction occurred at lower doses. The expression of collagen fibers and conexin-43 were increased in cardiac tissue in cisplatin-treated rats with doses of 2 and 3 mg/kg/week. The expression of endothelial nitric oxide synthase was also modified in cardiac and vascular tissues after cisplatin treatment. In conclusion, chronic cisplatin treatment provokes cardiac and vascular toxicity in a dose-dependent manner. Besides, vascular endothelial dysfunction occurs at lower doses than cardiac and systemic cardiovascular toxicity. Moreover, some structural changes in cardiac and vascular tissues are also patent even before any systemic cardiovascular alterations.

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Section: Discussionmentioning

confidence: 99%

Characterization of Cardiovascular Alterations Induced by Different Chronic Cisplatin Treatments

et al. 2017

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“…Therefore, targeting both energy pathways seems mandatory. This can be attained by using multi-site drugs such as the copper-based anti-cancer drugs termed casiopeinas, which inhibit glycolysis at the hexokinase level [33] and OXPHOS at the PDH 2 -OGDH and SDH levels [34,35]. However, the use of less-specific drugs may bring about undesirable side effects such as cardio-, nephro- and neurotoxicity, and anti-angiogenic activity affecting endothelial cells.…”

Section: Challenges Of the Warburg Effectmentioning

confidence: 99%

Warburg Effect or Reverse Warburg Effect? A Review of Cancer Metabolism

et al. 2015

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Cancer is a major threat to human health. A considerable amount of research has focused on elucidating the nature of cancer from its pathogenesis to treatment and prevention. Tumor cell metabolism has been considered a hallmark of cancer. Cancer cells differ from normal cells through unlimited cell division, and show a greater need for energy for their rapid growth and duplication. Research on glycometabolism, as the key point of energy metabolism, has played a unique role. In the 1920s, Warburg found that cancer cells prefer to produce adenosine triphosphate (ATP) by glycolysis, which is a less efficient pathway compared to oxidative phosphorylation. This striking discovery, called ‘the Warburg effect', has influenced and guided the study of the mechanism and treatment of tumors for generations, but its causal relationship with cancer progression is still unclear. Some studies have now shown contradicting evidence and a new hypothesis, the reverse Warburg effect, has been put forward, in which cancer cells produce most of their ATP via glycolysis, even under aerobic conditions. In this review we discuss the new points concerning the energy metabolism of a tumor, as well as the current facts and perspectives.

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“…The apoptosis observed might be the result of one or several signals which lead to this final effect. These signals could be mediated by generation of ROS [23], by the observed mitochondrial toxicity [24,27,28], or both, and might play, alone or cooperatively, an important role in the regulation of cell death induced by this type of complexes. Inhibition of respiration and ATP synthesis was observed in mitochondria as result of damage in several different mitochondrial sites in a dose-dependent manner, which compromises the energy dependent processes in cells [29].…”

Section: And [Cu(n-n)(oào)]nomentioning

confidence: 99%

Antiproliferative activity and QSAR study of copper(II) mixed chelate [Cu(N–N)(acetylacetonato)]NO3 and [Cu(N–N)(glycinato)]NO3 complexes, (Casiopeínas®)

Bravo-Gómez

García‐Ramos

Gracia-Mora

et al. 2009

Journal of Inorganic Biochemistry

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110

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Cardiotoxicity of copper-based antineoplastic drugs casiopeinas is related to inhibition of energy metabolism

Cited by 56 publications

References 26 publications

Characterization of Cardiovascular Alterations Induced by Different Chronic Cisplatin Treatments

Characterization of Cardiovascular Alterations Induced by Different Chronic Cisplatin Treatments

Warburg Effect or Reverse Warburg Effect? A Review of Cancer Metabolism

Antiproliferative activity and QSAR study of copper(II) mixed chelate [Cu(N–N)(acetylacetonato)]NO3 and [Cu(N–N)(glycinato)]NO3 complexes, (Casiopeínas®)

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