Document Detail


Gallic acid inhibits the growth of HeLa cervical cancer cells via apoptosis and/or necrosis.
MedLine Citation:
PMID:  20197077     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Gallic acid (GA) is widely distributed in various plants and foods, and its various biological effects have been reported. Here, we evaluated the effects of GA on HeLa cells in relation to cell growth inhibition and death. HeLa cell growth was diminished with an IC(50) of approximately 80 microM GA at 24h whereas an IC(50) of GA in human umbilical vein endothelial cells (HUVEC) was approximately 400 microM. GA-induced apoptosis and/or necrosis in HeLa cells and HUVEC, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsi(m)). The percentages of MMP (DeltaPsi(m)) loss cells and death cells were lower in HUVEC than HeLa cells. All the tested caspase inhibitors (pan-caspase, caspase-3, -8 or -9 inhibitor) significantly rescued HeLa cells from GA-induced cell death. GA increased reactive oxygen species (ROS) level and GSH (glutathione) depleted cell number in HeLa cells. Caspase inhibitors reduced GSH depleted cell number but not ROS level in GA-treated HeLa cells. In conclusion, GA inhibited the growth of HeLa cells and HUVEC via apoptosis and/or necrosis. The susceptibility of HeLa cells to GA was higher than that of HUVEC. GA-induced HeLa cell death was accompanied by ROS increase and GSH depletion.
Authors:
Bo Ra You; Hwa Jin Moon; Yong Hwan Han; Woo Hyun Park
Related Documents :
20846497 - Identification of pirnas in hela cells by massive parallel sequencing.
15770537 - In vitro inhibitory effect of flavonoids on growth, infection and vacuolation of helico...
9140967 - Yopk of yersinia pseudotuberculosis controls translocation of yop effectors across the ...
9499067 - Overexpression of c/ebpbeta represses human papillomavirus type 18 upstream regulatory ...
2948747 - Nuclear localization of type 1 aldosterone binding sites in steroid-unexposed gh3 cells.
9119887 - Separated human breast epithelial and myoepithelial cells have different growth factor ...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-01
Journal Detail:
Title:  Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association     Volume:  48     ISSN:  1873-6351     ISO Abbreviation:  Food Chem. Toxicol.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-04-14     Completed Date:  2010-07-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8207483     Medline TA:  Food Chem Toxicol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1334-40     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2010 Elsevier Ltd. All rights reserved.
Affiliation:
Department of Physiology, Medical School, Institute for Medical Sciences, Chonbuk National University, JeonJu, Republic of Korea.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adenocarcinoma / drug therapy*,  metabolism,  pathology
Antineoplastic Agents / pharmacology*
Apoptosis / drug effects*
Cell Survival / drug effects
Drug Screening Assays, Antitumor
Endothelium, Vascular / drug effects,  metabolism,  pathology
Female
Gallic Acid / pharmacology*
Glutathione / metabolism
Hela Cells
Humans
Membrane Potential, Mitochondrial / drug effects
Necrosis / chemically induced*
Superoxides / metabolism
Umbilical Veins / cytology
Uterine Cervical Neoplasms / drug therapy*,  metabolism,  pathology
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 11062-77-4/Superoxides; 149-91-7/Gallic Acid; 70-18-8/Glutathione

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Relationship of parental bonding styles with gray matter volume of dorsolateral prefrontal cortex in...
Next Document:  Carrier element-free coprecipitation (CEFC) method for separation and preconcentration of some metal...