Subcellular metabolite profiles of the parent CCRF-CEM and the derived CEM/C2 cell lines after treatment with doxorubicin

Anderson, Adrian B.

doi:10.1016/j.jchromb.2004.05.017

Cited by 20 publications

(24 citation statements)

References 33 publications

(42 reference statements)

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“…Further investigation of the distribution of ADR reveals the presence of specific sites of drug accumulation within the cell. Isolated mitochondria have been shown to effectively accumulate the drug (Anderson et al, 2004) and studies using perfused rat hearts have shown that ADR is localized primarily to the nucleus and mitochondria of the cell (Nicolay et al, 1986;Anderson et al, 2004;Tokarska-Schlattner et al, 2005).…”

Section: Pharmacokinetics Of Adrmentioning

confidence: 99%

Adriamycin-induced oxidative mitochondrial cardiotoxicity

2006

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The anticancer agent Adriamycin (ADR) has long been recognized to induce a dose-limiting cardiotoxicity. Numerous studies have attempted to characterize and elucidate the mechanism(s) behind its cardiotoxic effect. Despite a wealth of data covering a wide-range of effects mediated by the drug, the definitive mechanism remains a matter of debate. However, there is consensus that this toxicity is related to the induction of reactive oxygen species (ROS). Induction of ROS in the heart by ADR occurs via redox cycling of the drug at complex I of the electron transport chain. Many studies support the theory that mitochondria are a primary target of ADR-induced oxidative stress, both acutely and long-term. This review focuses on the effects of ADR redox cycling on the mitochondrion, which support the hypothesis that these organelles are indeed a major factor in ADR cardiotoxicity. This review has been constructed with particular emphasis on studies utilizing cardiac models with clinically relevant doses or concentrations of ADR in the hope of advancing our understanding of the mechanisms of ADR toxicity. This compilation of current data may reveal valuable insights for the development of therapeutic strategies better tailored to minimizing the dose-limiting effect of ADR.

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Section: Pharmacokinetics Of Adrmentioning

confidence: 99%

Adriamycin-induced oxidative mitochondrial cardiotoxicity

2006

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“…Human leukemia cells in passages 17 and 18 were treated with 25 mM DOX with treatment beginning 10 h after splitting. Viability was determined by Trypan Blue exclusion [18]. Human uterine sarcoma cells in passages 10-14 were treated with 25 mM DOX with treatment beginning 72 h after splitting.…”

Section: Doxorubicin Treatment and Viabilitymentioning

confidence: 99%

Separation of doxorubicin and doxorubicinol by cyclodextrin‐modified micellar electrokinetic capillary chromatography

2006

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Doxorubicinol (DOXol) is a human metabolite of the chemotherapy agent doxorubicin (DOX), and is associated with dose-dependent cardiotoxicity and decreased drug efficacy. Due to the structural similarities and equal molecular charges of DOXol and DOX, their electrophoretic separation is commonly ineffective. A method for separating and detecting DOX and DOXol, as well as two DOXol enantiomers, was established using cyclodextrin-modified micellar electrokinetic capillary chromatography with laser-induced fluorescence detection. Differential DOXol production was detected in a DOX-sensitive and resistant pair of cell lines, with a 0.08 +/- 0.01 fmol limit of detection.

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“…Drug determinations have been accomplished in plasma [117,138,141,142], urine [60,68,81], serum [79,117,[143][144][145], cerebral spinal fluid [141], and cell lines [125]. Impurity (and purity) analysis of drugs [18,59], preparations [146], and tablets [102,[147][148][149] have also been demonstrated with MEKC.…”

Section: Pharmaceuticalsmentioning

confidence: 99%

Recent advances in micellar electrokinetic chromatography

2005

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This review contains nearly 200 reference citations, and covers advances in electrokinetic capillary chromatography based on micelles, including stabilized micelle complexes, polymeric and mixed micelles from 2003-2004. Detection strategies, analyte determinations, and applications in micellar electrokinetic capillary chromatography (MEKC) are discussed. Information regarding methods of analyte concentration, analyte specific analyses, and nonstandard micelles has been summarized in tabular form to provide a means of rapid access to information pertinent to the reader.

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Subcellular metabolite profiles of the parent CCRF-CEM and the derived CEM/C2 cell lines after treatment with doxorubicin

Cited by 20 publications

References 33 publications

Adriamycin-induced oxidative mitochondrial cardiotoxicity

Adriamycin-induced oxidative mitochondrial cardiotoxicity

Separation of doxorubicin and doxorubicinol by cyclodextrin‐modified micellar electrokinetic capillary chromatography

Recent advances in micellar electrokinetic chromatography

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