Cardiotoxicity of cytotoxic drugs

Schimmel, Kirsten J. M.; Richel, Dick J.; Brink, R. B. A. van den; Guchelaar, Henk‐Jan

doi:10.1016/j.ctrv.2003.07.003

Cited by 328 publications

(249 citation statements)

References 69 publications

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“…One mechanism is based on the capacity of verapamil to inhibit the function of P-glycoprotein and therefore increase intracellular cytotoxic drug concentrations. This effect may be useful for cancer chemotherapy, but it could also lead to toxic effects in normal cells, such as cardiac cells [16] . However, some studies show increased doxorubicin accumulation in rat cardiomyocytes incubated in doxorubicin in combination with verapamil [18,19] .…”

Section: Introductionmentioning

confidence: 99%

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Oxidative modulation of marcaine and lekoptin in H9C2 rat myoblasts

et al. 2009

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Aim:The cytotoxicity of marcaine was estimated in combination with a calcium channel blocker. In addition, the influence of marcaine and marcaine plus lekoptin on a model system using the H9C2 cardiac cell line was investigated. Methods: Cells were incubated for five hours with marcaine, lekoptin, or with both drugs simultaneously. Apoptotic cells were detected using the TUNEL assay and the alkaline comet assay. Mitochondrial cell function after drug uptake was examined using the MTT assay. The concentration of MDA (malondialdehyde) -the final product of fatty-acid peroxidation, was quantified spectrophotometrically. The expression of glutathione S-transferase π (GST-π) was detected by immunofluorescence (IF) and Western blotting (WB) and inducible nitric oxide synthase (iNOS) was assessed by immunocytochemical staining (ABC). Results: Incubation with marcaine resulted in the highest number of apoptotic cells. After incubation with both marcaine and lekoptin, moderate damage to cells (54.2%±1.775% of DNA destruction) was observed. The highest levels of iNOS and GST-π expression were observed in cells treated with marcaine and marcaine plus lekoptin. The characteristic nuclear GST-π expression was observed in cells treated with both drugs. Conclusion: Lekoptin stimulated cells to proliferate. Marcaine caused membrane damage and ultimately cell death.

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Section: Introductionmentioning

confidence: 99%

“…Cardiotoxicity occurs during therapy with several cytotoxic drugs and may be the dose-limiting factor in treatment and cell response [16] . Lekoptin is often used for the treatment of ventricular arrhythmia and is a potent blocker of calcium channels.…”

Section: Introductionmentioning

confidence: 99%

Oxidative modulation of marcaine and lekoptin in H9C2 rat myoblasts

et al. 2009

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“…Все они в той или иной степени кар-диотоксичны (КТ) [13][14][15]. Наибольшее повреждающее воздействие на миокард оказывают антрациклиновые ан-тибиотики.…”

Section: терапевтический архив 7 2015unclassified

Late cardiotoxicity of high-dose chemotherapy according to the modified NHL-BFM-90 program in adult patients with diffuse large B-cell lymphoma

et al. 2015

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“…3). The most common hypothesis of doxorubicin-induced cardiotoxicity is the oxidative stress theory, where the principal toxic mechanisms involve iron and redox reactions [71]. It has been reported that when cardiomyocytes are exposed to doxorubicin, activation of the nuclear transcription factor NFkB and apoptosis occurred after redox cycling and formation of superoxide anion radicals and hydrogen peroxides [72].…”

Section: Pharmacology and Toxicity Of Doxorubicinmentioning

confidence: 99%