Journal
PHARMACOLOGICAL RESEARCH
Volume 103, Issue -, Pages 300-317Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2015.12.013
Keywords
Epigallocatechin-3-gallate; Menadione; Apoptosis; Mitochondrial dysfunction; Oxidative stress; Leukemia
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Funding
- Romanian National Authority for Scientific Research, CNCS-UEFISCDI [PN-II-ID-PCE-2011-3-0800]
- Sectoral Operational Programme Human Resources Development (SOP HRD)
- European Social Fund
- Romanian Government [POS-DRU/187/1.5/S/156069]
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We have investigated the growth-suppressive action of epigallocatechin-3-gallate (EGCG) on human leukemia Jurkat T cells. Results show a strong correlation between the dose-dependent reduction of clonogenic survival following acute EGCG treatments and the EGCG-induced decline of the mitochondrial level of Ca2+. The cell killing ability of EGCG was synergistically enhanced by menadione. In addition, the cytotoxic effect of EGCG applied alone or in combination with menadione was accompanied by apoptosis induction. We also observed that in acute treatments EGCG displays strong antioxidant properties in the intracellular milieu, but concurrently triggers some oxidative stress generating mechanisms that can fully develop on a longer timescale. In parallel, EGCG dose-dependently induced mitochondria] depolarization during exposure, but this condition was subsequently reversed to a persistent hyperpolarized mitochondrial state that was dependent on the activity of respiratory Complex I. Fluorimetric measurements suggest that EGCG is a mitochondrial Complex III inhibitor and indicate that EGCG evokes a specific cellular fluorescence with emission at 400 nm and two main excitation bands (at 330 nm and 350 nm) that may originate from a mitochondrial supercomplex containing dimeric Complex III and dimeric ATP-synthase, and therefore could provide a valuable means to characterize the functional properties of the respiratory chain. (C) 2015 Elsevier Ltd. All rights reserved.
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