Document Detail

The anti-apoptotic effects of caspase inhibitors on propyl gallate-treated HeLa cells in relation to reactive oxygen species and glutathione levels.
MedLine Citation:
PMID:  19434396     Owner:  NLM     Status:  MEDLINE    
Propyl gallate (PG) as a synthetic antioxidant is widely used in processed food, cosmetics and medicinal preparations. Despite the assumed low toxicity of PG, it exerts a variety of effects on tissue and cell functions. In the present study, we evaluated the anti-apoptotic effects of caspase inhibitors on PG-treated human cervix adenocarcinoma HeLa cells in relation to the changes of reactive oxygen species (ROS) and glutathione (GSH) levels. PG induced apoptosis in a dose-dependent manner, as evidenced by sub-G1 cells and annexin V staining cells. Treatment with pan-caspase inhibitor, caspase-3 inhibitor, caspase-8 inhibitor or caspase-9 inhibitor significantly prevented apoptosis in PG-treated HeLa cells at 24 h. The intracellular ROS levels including O (2) (*-) were increased or decreased in PG-treated HeLa cells depending on the incubation times (1 or 24 h). PG depleted intracellular GSH content in HeLa cells at 24 h. Treatment with caspase inhibitor reduced ROS levels and significantly prevented GSH depletion in PG-treated HeLa cells at 24 h. In conclusion, PG induced apoptosis in HeLa cells. The anti-apoptotic effect of caspase inhibitor on PG-induced HeLa cell death was closely related to the reduction of ROS levels, especially mitochondrial O (2) (*-) , as well as to the inhibition of GSH depletion.
Yong Hwan Han; Hwa Jin Moon; Bo Ra You; Woo Hyun Park
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-05-12
Journal Detail:
Title:  Archives of toxicology     Volume:  83     ISSN:  1432-0738     ISO Abbreviation:  Arch. Toxicol.     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-08-03     Completed Date:  2009-11-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0417615     Medline TA:  Arch Toxicol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  825-33     Citation Subset:  IM    
Department of Physiology, Centers for Healthcare Technology Development, Institute for Medical Sciences, Chonbuk National University, Jeonju, Republic of Korea.
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MeSH Terms
Amino Acid Chloromethyl Ketones / pharmacology
Annexin A5 / metabolism
Antioxidants / pharmacology
Apoptosis / drug effects*
Caspase 3 / metabolism
Caspase 8 / metabolism
Caspase 9 / metabolism
Caspases / antagonists & inhibitors*
Dose-Response Relationship, Drug
Enzyme Inhibitors / pharmacology
G1 Phase / drug effects
Glutathione / metabolism*
Hela Cells
Oligopeptides / pharmacology
Propyl Gallate / pharmacology*
Reactive Oxygen Species / metabolism*
Time Factors
Reg. No./Substance:
0/Amino Acid Chloromethyl Ketones; 0/Annexin A5; 0/Antioxidants; 0/Enzyme Inhibitors; 0/Oligopeptides; 0/Reactive Oxygen Species; 0/benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone; 0/benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone; 0/benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone; 0/benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 121-79-9/Propyl Gallate; 70-18-8/Glutathione; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 8; EC 3.4.22.-/Caspase 9; EC 3.4.22.-/Caspases

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

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