The antioxidant caffeic acid phenethyl ester induces apoptosis associated with selective scavenging of hydrogen peroxide in human leukemic HL-60 cells

Citation
Yj. Chen et al., The antioxidant caffeic acid phenethyl ester induces apoptosis associated with selective scavenging of hydrogen peroxide in human leukemic HL-60 cells, ANTI-CANC D, 12(2), 2001, pp. 143-149
Citations number
32
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology,"Onconogenesis & Cancer Research
Journal title
ANTI-CANCER DRUGS
ISSN journal
0959-4973 → ACNP
Volume
12
Issue
2
Year of publication
2001
Pages
143 - 149
Database
ISI
SICI code
0959-4973(200102)12:2<143:TACAPE>2.0.ZU;2-I
Abstract
Caffeic acid phenethyl ester (CAPE), an active component of propolis, has m any biological and pharmacological activities including antioxidation and t umor cell cytotoxicity. We examined the type of cell death in human leukemi c HL-60 cells after CAFE treatment in order to elucidate the relationship b etween CAFE-induced alterations of the redox state and apoptosis. CAFE trea tment (6 mug/ml) resulted in marked growth inhibition up to 70.3 +/- 4.0% a t day 2. This inhibition was partially blocked by pretreatment with N-acety l-L-cycteine (NAC), Agarose gel electrophoresis showed evident DNA fragment ation after CAFE treatment. CAFE induced a significant decrease in mitochon drial transmembrane potential to about halt of the untreated level after 6 h and a rapid depletion of intracellular glutathione (GSH) down to 41.7 +/- 6.0% after 1 h. Pretreatment of HL-60 cells with NAC reversed the GSH depl etion and partially rescued cells from CAPE-induced apoptosis. With regard to intracellular reactive oxygen species, CAFE caused a fast and profound s cavenging of H2O2 (19% of untreated cells after a 2-h treatment) but not of superoxide anion. These results suggest that apoptosis induced by CAFE is associated with mitochondrial dysfunction, GSH depletion and selective scav enging of H2O2 in human leukemic HL-60 cells. [(C) 2001 Lippincott Williams & Wilkins.].