Study on caspase-induced mitochondrial dysfunction by anticancer drugs

Zhimin Tao; Matthew P. Morrow; Harvey S. Penefsky; Jerry Goodisman; Abdul Kader Souid

doi:10.2174/157488507781695621

Study on caspase-induced mitochondrial dysfunction by anticancer drugs

Zhimin Tao, Matthew P. Morrow, Harvey S. Penefsky, Jerry Goodisman, Abdul Kader Souid

Research output: Contribution to journal › Article › peer-review

2 Citations (Scopus)

Abstract

Apoptosis, induced in tumors by anticancer agents, is characterized by caspase activation, impaired cellular respiration and decreased cellular ATP. Respiration in Jurkat and HL-60 cells treated with doxorubicin, dactinomycin or platinum drugs is measured using a Pd(II) phosphor that monitors [O₂ ] in cell suspensions as a function of time. Cellular ATP is determined using the luciferin-luciferase bioluminescence system. Intracellular caspase activation is measured by allowing caspases to cleave Ac-DEVD-AFC to the fluorescent AFC, which is detected on HPLC. Comparing the ways in which respiration, ATP level, and caspase activity vary with time points up differences between the mechanisms of actions of doxorubicin, dactinomycin and the platinum compounds. These methods accurately determine the sensitivity of tumors to anticancer drugs.

Original language	English
Pages (from-to)	233-235
Number of pages	3
Journal	Current Drug Therapy
Volume	2
Issue number	3
DOIs	https://doi.org/10.2174/157488507781695621
Publication status	Published - 2007
Externally published	Yes

ASJC Scopus subject areas

Pharmacology, Toxicology and Pharmaceutics(all)
Pharmacology (medical)

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title = "Study on caspase-induced mitochondrial dysfunction by anticancer drugs",

abstract = "Apoptosis, induced in tumors by anticancer agents, is characterized by caspase activation, impaired cellular respiration and decreased cellular ATP. Respiration in Jurkat and HL-60 cells treated with doxorubicin, dactinomycin or platinum drugs is measured using a Pd(II) phosphor that monitors [O2 ] in cell suspensions as a function of time. Cellular ATP is determined using the luciferin-luciferase bioluminescence system. Intracellular caspase activation is measured by allowing caspases to cleave Ac-DEVD-AFC to the fluorescent AFC, which is detected on HPLC. Comparing the ways in which respiration, ATP level, and caspase activity vary with time points up differences between the mechanisms of actions of doxorubicin, dactinomycin and the platinum compounds. These methods accurately determine the sensitivity of tumors to anticancer drugs.",

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T1 - Study on caspase-induced mitochondrial dysfunction by anticancer drugs

AU - Tao, Zhimin

AU - Morrow, Matthew P.

AU - Penefsky, Harvey S.

AU - Goodisman, Jerry

AU - Souid, Abdul Kader

PY - 2007

Y1 - 2007

N2 - Apoptosis, induced in tumors by anticancer agents, is characterized by caspase activation, impaired cellular respiration and decreased cellular ATP. Respiration in Jurkat and HL-60 cells treated with doxorubicin, dactinomycin or platinum drugs is measured using a Pd(II) phosphor that monitors [O2 ] in cell suspensions as a function of time. Cellular ATP is determined using the luciferin-luciferase bioluminescence system. Intracellular caspase activation is measured by allowing caspases to cleave Ac-DEVD-AFC to the fluorescent AFC, which is detected on HPLC. Comparing the ways in which respiration, ATP level, and caspase activity vary with time points up differences between the mechanisms of actions of doxorubicin, dactinomycin and the platinum compounds. These methods accurately determine the sensitivity of tumors to anticancer drugs.

AB - Apoptosis, induced in tumors by anticancer agents, is characterized by caspase activation, impaired cellular respiration and decreased cellular ATP. Respiration in Jurkat and HL-60 cells treated with doxorubicin, dactinomycin or platinum drugs is measured using a Pd(II) phosphor that monitors [O2 ] in cell suspensions as a function of time. Cellular ATP is determined using the luciferin-luciferase bioluminescence system. Intracellular caspase activation is measured by allowing caspases to cleave Ac-DEVD-AFC to the fluorescent AFC, which is detected on HPLC. Comparing the ways in which respiration, ATP level, and caspase activity vary with time points up differences between the mechanisms of actions of doxorubicin, dactinomycin and the platinum compounds. These methods accurately determine the sensitivity of tumors to anticancer drugs.

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Study on caspase-induced mitochondrial dysfunction by anticancer drugs

Abstract

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