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Current Drug Therapy

Editor-in-Chief

ISSN (Print): 1574-8855
ISSN (Online): 2212-3903

Study on Caspase-Induced Mitochondrial Dysfunction by Anticancer Drugs

Author(s): Zhimin Tao, Matthew P. Morrow, Harvey S. Penefsky, Jerry Goodisman and Abdul-Kader Souid

Volume 2, Issue 3, 2007

Page: [233 - 235] Pages: 3

DOI: 10.2174/157488507781695621

Price: $65

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.

Keywords: Apoptosis, cellular ATP, 7-amino-4-trifluoromethyl coumarin, pan-caspase inhibitor, doxorubicin


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