Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/12625
Title: Mitochondrially targeted effects of berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 mouse melanoma cells: comparison with direct effects on isolated mitochondrial fractions
Authors: Pereira, Gonçalo C. 
Branco, Ana F. 
Matos, Júlio A. C. 
Pereira, Sandro L. 
Parke, Donna 
Perkins, Edward L. 
Serafim, Teresa L. 
Sardão, Vilma A. 
Santos, Maria S. 
Moreno, Antonio J. M. 
Holy, Jon 
Oliveira, Paulo J. 
Issue Date: Nov-2007
Publisher: The American Society for Pharmacology and Experimental Therapeutics
Citation: Journal of Pharmacology and Experimental Therapeutics. 323:2 (2007) 636-649
Abstract: Berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a)quinolizinium] is an alkaloid present in plant extracts and has a history of use in traditional Chinese and Native American medicine. Because of its ability to arrest the cell cycle and cause apoptosis of several malignant cell lines, it has received attention as a potential anticancer therapeutic agent. Previous studies suggest that mitochondria may be an important target of berberine, but relatively little is known about the extent or molecular mechanisms of berberine-mitochondrial interactions. The objective of the present work was to investigate the interaction of berberine with mitochondria, both in situ and in isolated mitochondrial fractions. The data show that berberine is selectively accumulated by mitochondria, which is accompanied by arrest of cell proliferation, mitochondrial fragmentation and depolarization, oxidative stress, and a decrease in ATP levels. Electron microscopy of berberine-treated cells shows a reduction in mitochondria-like structures, accompanied by a decrease in mitochondrial DNA copy number. Isolated mitochondrial fractions treated with berberine had slower mitochondrial respiration, especially when complex I substrates were used, and increased complex I-dependent oxidative stress. It is also demonstrated for the first time that berberine stimulates the mitochondrial permeability transition. Direct effects on ATPase activity were not detected. The present work demonstrates a number of previously unknown alterations of mitochondrial physiology induced by berberine, a potential chemotherapeutic agent, although it also suggests that high doses of berberine should not be used without a proper toxicology assessment
URI: http://hdl.handle.net/10316/12625
ISSN: 0022-3565
Rights: openAccess
Appears in Collections:FCTUC Ciências da Vida - Artigos em Revistas Internacionais

Files in This Item:
File Description SizeFormat
Mitochondrially targeted effects of berberine.pdf538.98 kBAdobe PDFView/Open
Show full item record

Page view(s)

134
checked on Oct 15, 2019

Download(s) 5

2,030
checked on Oct 15, 2019

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.