Pre-administration of docetaxel protects against adriamycin-induced cardiotoxicity

Sakaguchi, Hiromi; Kodama, Ayumi; Tomonari, Mari; Ando, Yumiko; Tabuchi, Mayumi; To, Hideto; Araki, Ryosuke; Kitahara, Takashi; Sasaki, Hidetada; Ohdo, Shigehiro; Higuchi, Shun

doi:10.1007/s10549-007-9667-8

Cited by 9 publications

(20 citation statements)

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“…A subsequent study r evealed t hat the t oxic d eath of m ouse was a ttributed to cardiotoxicity induced by ADR [16]. Therefore, in this study, the differential proteomic profiling of mouse heart tissues from DOC-ADR, ADR&DOC, and control groups was performed to identify the proteins that mediate the cardioprotective effect of DOC pretreatment in the DOC-ADR group.…”

Section: Discussionmentioning

confidence: 99%

“…The ADR dose had been shown to be cardiotoxic in mouse [27]. The DOC dose had been shown to provide the strongest cardioprotection in the intermittent-dosing m ouse g roup [16]. Also, w hen dos ing i ntervals ( 6, 12, 24 h) be tween DOC and ADR treatments were changed, 12-h interval group showed the lowest toxic death rate [16].…”

Section: Animal Treatment and Tissue Processingmentioning

confidence: 99%

“…The DOC dose had been shown to provide the strongest cardioprotection in the intermittent-dosing m ouse g roup [16]. Also, w hen dos ing i ntervals ( 6, 12, 24 h) be tween DOC and ADR treatments were changed, 12-h interval group showed the lowest toxic death rate [16]. Heart samples were isolated from all mice 1 week after ADR was administered in the ADR&DOC and D OC-ADR gr oups.…”

Section: Animal Treatment and Tissue Processingmentioning

confidence: 99%

“…This remarkable finding has been subsequently studied in detail using mouse models [15,16], and t he r eduction i n t oxic de ath w as f ound t o b e DOC dose-dependent [ 16]; how ever, no 5 mechanism explaining the effect of DOC pre-administration has been established.…”

Section: Introductionmentioning

confidence: 99%

“…Chronotherapy i s de fined a s t he administration o f me dications u sing biological rhythms to o ptimize therapeutic outcomes and/or control adverse effect. The chronopharmacology of many antitumor drugs have been studied in human and animals specifically to decrease adverse effects [5][6][7][8][9][10][11][12][13][14][15][16]. The individual toxicities of ADR and DOC apparently depend on dos ing time in animals and human [8][9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

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A toxicoproteomic study on cardioprotective effects of pre-administration of docetaxel in a mouse model of adriamycin-induced cardiotoxicity

Ohyama

Tomonari

Ichibangase

et al. 2010

Biochemical Pharmacology

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Studies s uggest t hat pr e-administration o f d ocetaxel ( DOC) in a driamycin ( ADR)-analysis o f h eart t issue from control, intermittent-dosing (DOC-ADR), and s imultaneous -dosing (ADR&DOC) groups. In DOC-ADR group, ADR was administered 12 h after DOC injection; i n A DR&DOC g roup, bot h dr ugs w ere a dministered s imultaneously; i n control group, saline was administered at the same timing as ADR injection of other groups. Heart samples were isolated from all mice 1 week after the treatment. The highly reproducible and sensitive method (FD-LC-MS/MS) identified nine proteins that were differentially expressed in heart tissue of control and the two treatment groups; seven of these nine proteins participate in cellular energy production pathways, including glycolysis, the tricarboxylic acid cycle, and the mit ochondrial electron t ransport c hain.Significantly higher e xpression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was observed in the DOC-ADR group, the g roup with the fewer cardiotoxic de aths, t han in the ADR&DOC group. Therefore, GAPDH may have potential as a drug target for protective intervention and a biomarker for 3 evaluation of the cardioprotective effects in pre-clinical studies.

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Section: Discussionmentioning

confidence: 99%

Section: Animal Treatment and Tissue Processingmentioning

confidence: 99%

Section: Animal Treatment and Tissue Processingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

A toxicoproteomic study on cardioprotective effects of pre-administration of docetaxel in a mouse model of adriamycin-induced cardiotoxicity

Ohyama

Tomonari

Ichibangase

et al. 2010

Biochemical Pharmacology

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Reduced in vivo high-energy phosphates precede Adriamycin-induced cardiac dysfunction

Maslov

Chacko

Hirsch³

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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is an established, life-saving antineoplastic agent, the use of which is often limited by cardiotoxicity. ADR-induced cardiomyopathy is often accompanied by depressed myocardial high-energy phosphate (HEP) metabolism. Impaired HEP metabolism has been suggested as a potential mechanism of ADR cardiomyopathy, in which case the bioenergetic decline should precede left ventricular (LV) dysfunction. We tested the hypothesis that murine cardiac energetics decrease before LV dysfunction following ADR (5 mg/kg ip, weekly, 5 injections) in the mouse. As a result, the mean myocardial phosphocreatine-to-ATP ratio (PCr/ATP) by spatially localized 31 P magnetic resonance spectroscopy decreased at 6 wk after first ADR injection (1.79 Ϯ 0.18 vs. 1.39 Ϯ 0.30, means Ϯ SD, control vs. ADR, respectively, P Ͻ 0.05) when indices of systolic and diastolic function by magnetic resonance imaging were unchanged from control values. At 8 wk, lower PCr/ATP was accompanied by a reduction in ejection fraction (67.3 Ϯ 3.9 vs. 55.9 Ϯ 4.2%, control vs. ADR, respectively, P Ͻ 0.002) and peak filling rate (0.56 Ϯ 0.12 vs. 0.30 Ϯ 0.13 l/ms, control vs. ADR, respectively, P Ͻ 0.01). PCr/ATP correlated with peak filling rate and ejection fraction, suggesting a relationship between cardiac energetics and both LV systolic and diastolic dysfunction. In conclusion, myocardial in vivo HEP metabolism is impaired following ADR administration, occurring before systolic or diastolic abnormalities and in proportion to the extent of eventual contractile abnormalities. These observations are consistent with the hypothesis that impaired HEP metabolism contributes to ADRinduced myocardial dysfunction. magnetic resonance imaging; 31 P spectroscopy ADRIAMYCIN (ADR) represents one of the most potent and extensively used anticancer drugs (46); however, its antineoplastic use can be compromised in practice by cardiotoxic side effects (17,35). Although ADR-induced cardiotoxicity is usually subclinical, symptoms of heart failure (HF) can develop acutely during therapy (18, 33) or chronically (25,34). In general, HF with systolic and diastolic abnormalities develops in 18 -36% of patients receiving a cumulative ADR dose of 250 -601 mg/m 2 (17, 35). A spectrum of cardiac metabolic (21, 39) and morphological (2, 6) abnormalities occurs following ADR treatment, but it is unclear which, if any of these, causes ADR cardiotoxicity. One metabolic abnormality that may contribute mechanistically to ADR cardiotoxicity is impaired creatine kinase (CK) energetics.The CK reaction serves as the prime cardiac energy reservoir, quickly and reversibly converting adenosine diphosphate and phosphocreatine (PCr) to ATP and creatine (15,44), where the PCr-to-ATP ratio (PCr/ATP) is commonly used to characterize a high-energy phosphate metabolism. An inhibition of CK impairs cardiac function or contractile reserve in normal hearts (13, 37), and an altered CK metabolism is observed in both experimental and human HF (14,19,23,32,47). In particular, an altered in vitro and in vivo CK energetics ...

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Recent Advances in Protection against Doxorubicin-induced Toxicity

Injac

Štrukelj

2008

Technol Cancer Res Treat

124

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Anthracycline antibiotics are among the most effective and commonly used anticancer drugs.Unfortunately, their clinical use is restricted by dose-dependent toxicity. Doxorubicin is an anthracycline antibiotic and cytotoxic (antineoplastic) agent. It is commonly used against ovarian, breast, lung, uterine and cervical cancers, Hodgkin's disease, soft tissue and primary bone sarcomas, as well against in several other cancer types. It has been shown that free radicals are involved in doxorubicin-induced toxicity. Doxorubicin causes the generation of free radicals and the induction of oxidative stress, associated with cellular injury. This review illustrates recent applications of different natural products, drugs, drug delivery systems, and approaches for protection against doxorubicin-induced toxicity (2006-present).Key words: Doxorubicin; Toxicity; Oxidative stress; Antioxidants; Natural products; Drugs; Drug delivery systems; Nanooncology; Liposomes; Targeting cancer. IntroductionDoxorubicin (Dox) is one of the most potent broad-spectrum antitumor anthracycline antibiotics, widely used to treat a variety of cancers, including severe leukemias, lymphomas, and solid tumors (1), in combination with different drugs (Table I). On the other hand, the clinical use of Dox is restricted because of its serious toxicity, which frequently leads to irreversible degenerative cardiomyopathy and heart failure (2-4). The cytotoxic effect of Dox on malignant cells and its toxic effects on various organs (heart, liver, lung, kidney, blood cells, and testis) are thought to be related to the nucleotide base intercalation and the cell membrane lipid-binding activities of Dox (5-7). Despite that, the precise mechanisms have not been fully established, and optimal therapeutic approaches for organo-protection remain undefined (8).During the past decade, considerable progress has been made in investigating a protective role against doxorubicin-induced toxicity. There are many different approaches, agents and designs that have been tested for protecting in vivo-in vitro cells treated with Dox (9-15). Doxorubicin-induced ToxicityIn 1976, a new ATP-requiring enzyme, DNA gyrase, was discovered in bacterial cells. It has the property of being able to change the topology of closed circular duplex DNA. DNA gyrase was found to have a crucial role in DNA replication, and for being able to pass one strand of DNA through another. solved the problems of how DNA could be rapidly unwound during replication and how the daughter DNA strands could be separated after replication. Two main classes of enzymes were found in subsequent studies of mammalian cells. The first enzyme (topoisomerase I) changed DNA topology by breaking and rejoining a single DNA strand, while the second (topoisomerase II), with some of the characteristics of bacterial gyrase, broke both strands of one double-stranded DNA to allow passage of a second double-helical strand through the breakage point. The findings of the DNA topoisomerases also explained a problem regarding th...

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Pre-administration of docetaxel protects against adriamycin-induced cardiotoxicity

Abstract: We conclude that pre-administration of DOC may protect against ADR-induced toxic death and cardiotoxicity.

Cited by 9 publications

References 24 publications

A toxicoproteomic study on cardioprotective effects of pre-administration of docetaxel in a mouse model of adriamycin-induced cardiotoxicity

A toxicoproteomic study on cardioprotective effects of pre-administration of docetaxel in a mouse model of adriamycin-induced cardiotoxicity

Reduced in vivo high-energy phosphates precede Adriamycin-induced cardiac dysfunction

Recent Advances in Protection against Doxorubicin-induced Toxicity

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