Volume 5, Issue 3(Suppl)
Biochem Anal Biochem 2016
ISSN: 2161-1009, Biochem an open access journal
Page 61
Biochemistry 2016
October 10-12, 2016
conferenceseries
.com
Biochemistry
October 10-12, 2016 Kuala Lumpur, Malaysia
International Conference on
Targeting of increased copper level in diethylnitrosamine (DEN) induced hepatocellular carcinoma cells in
rats by epigallocatechin-3-gallate (EGCG)
Sheikh Mumtaz Hadi
Aligarh Muslim University, India
T
o account for the observed anticancer properties of plant polyphenols, we have proposed a mechanism which involves the
mobilization of endogenous copper ions by polyphenols leading to the generation of reactive oxygen species (ROS) that serve
as proximal DNA cleaving agents. Over the last decade, we have proceeded to validate our hypothesis with considerable success.
For example, polyphenol induced growth inhibition in breast cancer cell lines is inhibited by copper chelators and copper overload
in lymphocytes leads to increased cellular DNA degradation by polyphenols. As a further confirmation of our hypothesis, we have
induced hepatocellular carcinoma in rats by diethylnitrosamine (DEN). The induction of carcinoma was confirmed by visual
examination of liver and various liver cancer markers. 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. This is further
confirmation of the increased copper levels in such cells. 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 desferrioxamine mesylate and histidine respectively were also ineffective in inhibiting EGCG mediated DNA
breakage.
saimasalman50@yahoo.comBiochem Anal Biochem 2016, 5:3(Suppl)
http://dx.doi.org/10.4172/2161-1009.S1.006