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Bio Summit & Molecular Biology 2016
October 10-12, 2016
Volume 6, Issue 6(Suppl)
J Biotechnol Biomater
ISSN: 2155-952X JBTBM, an open access journal
conferenceseries
.com
October 10-12, 2016 Dubai, UAE
2
nd
World Congress on
Bio Summit & Molecular Biology Expo
Yuebin Ke et al., J Biotechnol Biomater 2016, 6:6(Suppl)
http://dx.doi.org/10.4172/2155-952X.C1.062Compensatory effects of
hOGG1
for
hMTH1
in oxidative DNAdamage caused by hydrogen peroxide
Yuebin Ke and Ziquan Lv
Shenzhen Center for Disease Control and Prevention, China
T
his study aimed to investigate the potential compensatory effects of
hOGG1
and
hMTH1
in the repair of oxidative DNA
damage. The
hOGG1
and
hMTH1
gene knockdown human embryonic pulmonary fibroblast cell lines were established
by Lentivirus-mediated RNA interference. The messenger RNA (mRNA) levels of
hOGG1
and hM1TH1 were analyzed by
the real-time polymerase chain reaction and 8-hydroxy-20-deoxyguanosine (8-oxo-dG) formation was analyzed in a high-
performance liquid chromatography-electrochemical detection system. The
hOGG1
and
hMTH1
knockdown cells were
obtained through blasticidin selection. After transfection of
hOGG1
and
hMTH1
small interfering RNA, the expression levels
of the mRNA of
hOGG1
and
hMTH1
genes were decreased by 97.2% and 96.2%, respectively. The cells then were exposed to
100 mmol/L of hydrogen peroxide (H
2
O
2
) for 12 hours to induce oxidative DNA damage. After H
2
O
2
exposure,
hMTH1
mRNA
levels were increased by 25% in
hOGG1
gene knockdown cells, whereas
hOGG1
mRNA levels were increased by 52% in
hMTH1
gene knockdown cells. Following the treatment with H
2
O
2
, the 8-oxo-dG levels in the DNA of
hOGG1
gene knockdown cells
were 3.1-fold higher than those in untreated HFL cells and 1.67-fold higher than those in H
2
O
2
-treated wild-type cells. The
8-oxo-dG levels in
hMTH1
gene knockdown cells were 2.3-fold higher than those in untreated human embryonic pulmonary
fibroblast cells but did not differ significantly from those in H
2
O
2
-treated wild-type cells. Our data suggested that
hOGG1
could
compensate for
hMTH1
during oxidative DNA damage caused by H
2
O
2
, whereas
hMTH1
could not compensate sufficiently
for
hOGG1
during the process.
Biography
Yuebin Ke is a Professor of the Shenzhen Center for Disease Control and Prevention and an Adjunct Professor of Life Sciences at Shenzhen University. He has
completed his PhD from Huazhong University of Science and Technology and Postdoctoral studies from Virginia Polytechnic Institute and State University. He has
published 18 papers in the areas of environmental health and molecular biology.
keyke@szu.edu.cn