NDLI: Targeting increased copper levels in diethylnitrosamine induced hepatocellular carcinoma cells in rats by epigallocatechin-3-gallate.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Farhan, Mohd Rizvi, Asim Naseem, Imrana Hadi, S. M. Ahmad, Aamir
Description	Country affiliation: India Author Affiliation: Farhan M ( Department of Biochemistry, Faculty of Life Sciences, AMU, Aligarh, India.); Rizvi A ( Department of Biochemistry, Faculty of Life Sciences, AMU, Aligarh, India.); Naseem I ( Section of Radiobiology, Department of Radiology, The Biomedical Research Tower, The Ohio State University, 460W 12th Avenue, Columbus, OH, USA.); Hadi SM ( Department of Biochemistry, Faculty of Life Sciences, AMU, Aligarh, India.); Ahmad A ( Department of Biochemistry, Faculty of Life Sciences, AMU, Aligarh, India.)
Abstract	We have earlier elucidated a pathway for the anticancer action of plant polyphenolic compounds against malignant cells involving mobilisation of endogenous copper ions and the consequent prooxidant action. To further confirm our hypothesis in vivo, we induced hepatocellular carcinoma (HCC) in rats by diethylnitrosamine (DEN). We show that in such carcinoma cells, there is a progressive elevation in copper levels at various intervals after DEN administration. Concurrently with increasing copper levels, epigallocatechin-3-gallate (EGCG; a potent anticancer plant polyphenol found in green tea) mediated DNA breakage in malignant cells is also increased. The cell membrane permeable copper chelator neocuproine inhibited the EGCG-mediated cellular DNA degradation, whereas the membrane impermeable chelator bathocuproine was ineffective. Iron and zinc specific chelators desferoxamine mesylate and histidine, respectively, were also ineffective in inhibiting EGCG mediated DNA breakage. Through the use of specific scavengers, the mechanism of DNA breakage was determined to be mediated by reactive oxygen species. In summary, we provide an in vivo evidence of accumulating copper in hepatocellular carcinoma that is targeted by EGCG, leading to its anticancer role in a prooxidant manner. Our findings confirm a novel mechanism of anticancer activity of EGCG in particular and plant derived nutraceuticals in general.
File Format	HTM / HTML
ISSN	10104283
Issue Number	11
Volume Number	36
e-ISSN	14230380
Journal	Tumor Biology
Language	English
Publisher	Springer
Publisher Date	2015-11-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Subject Keyword	Discipline Medicine__semicolon__oncology Carcinoma, Hepatocellular Drug Therapy Catechin Analogs & Derivatives Copper Metabolism Liver Neoplasms Animals Chemically Induced Pathology Administration & Dosage Chemistry Cell Membrane Permeability Drug Effects Dna Damage Diethylnitrosamine Toxicity Free Radical Scavengers Humans Oxidative Stress Rats Reactive Oxygen Species Tea Journal Article
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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