PMID- 26823956
OWN - NLM
STAT- MEDLINE
DA  - 20160129
DCOM- 20161213
LR  - 20170220
IS  - 1942-0994 (Electronic)
IS  - 1942-0994 (Linking)
VI  - 2016
DP  - 2016
TI  - Oxidative Stress and Carbonyl Lesions in Ulcerative Colitis and Associated
Colorectal Cancer.
PG  - 9875298
LID - 10.1155/2016/9875298 [doi]
AB  - Oxidative stress has long been known as a pathogenic factor of ulcerative colitis
(UC) and colitis-associated colorectal cancer (CAC), but the effects of secondary
carbonyl lesions receive less emphasis. In inflammatory conditions, reactive
oxygen species (ROS), such as superoxide anion free radical (O2 (-)), hydrogen
peroxide (H2O2), and hydroxyl radical (HO()), are produced at high levels and
accumulated to cause oxidative stress (OS). In oxidative status, accumulated ROS
can cause protein dysfunction and DNA damage, leading to gene mutations and cell
death. Accumulated ROS could also act as chemical messengers to activate
signaling pathways, such as NF-kappaB and p38 MAPK, to affect cell proliferation,
differentiation, and apoptosis. More importantly, electrophilic carbonyl
compounds produced by lipid peroxidation may function as secondary pathogenic
factors, causing further protein and membrane lesions. This may in turn
exaggerate oxidative stress, forming a vicious cycle. Electrophilic carbonyls
could also cause DNA mutations and breaks, driving malignant progression of UC.
The secondary lesions caused by carbonyl compounds may be exceptionally important
in the case of host carbonyl defensive system deficit, such as aldo-keto
reductase 1B10 deficiency. This review article updates the current understanding
of oxidative stress and carbonyl lesions in the development and progression of UC
and CAC.
FAU - Wang, Zhiqi
AU  - Wang Z
AD  - Department of Pharmacology, Division of Stem Cell Regulation and Application,
State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan
(Incubation), and Key Laboratory of Colleges and Universities in Hunan Province
for Cytobiology and Molecular Biotechnology, Hunan University of Chinese
Medicine, Changsha, Hunan 410208, China.
FAU - Li, Sai
AU  - Li S
AD  - Department of Pharmacology, Division of Stem Cell Regulation and Application,
State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan
(Incubation), and Key Laboratory of Colleges and Universities in Hunan Province
for Cytobiology and Molecular Biotechnology, Hunan University of Chinese
Medicine, Changsha, Hunan 410208, China.
FAU - Cao, Yu
AU  - Cao Y
AD  - Department of Medical Microbiology, Immunology & Cell Biology, Simmons Cancer
Institute, Southern Illinois University School of Medicine, 913 N. Rutledge
Street, Springfield, IL 62794, USA.
FAU - Tian, Xuefei
AU  - Tian X
AD  - Department of Pharmacology, Division of Stem Cell Regulation and Application,
State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan
(Incubation), and Key Laboratory of Colleges and Universities in Hunan Province
for Cytobiology and Molecular Biotechnology, Hunan University of Chinese
Medicine, Changsha, Hunan 410208, China.
FAU - Zeng, Rong
AU  - Zeng R
AD  - Department of Pharmacology, Division of Stem Cell Regulation and Application,
State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan
(Incubation), and Key Laboratory of Colleges and Universities in Hunan Province
for Cytobiology and Molecular Biotechnology, Hunan University of Chinese
Medicine, Changsha, Hunan 410208, China.
FAU - Liao, Duan-Fang
AU  - Liao DF
AD  - Department of Pharmacology, Division of Stem Cell Regulation and Application,
State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan
(Incubation), and Key Laboratory of Colleges and Universities in Hunan Province
for Cytobiology and Molecular Biotechnology, Hunan University of Chinese
Medicine, Changsha, Hunan 410208, China.
FAU - Cao, Deliang
AU  - Cao D
AD  - Department of Pharmacology, Division of Stem Cell Regulation and Application,
State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan
(Incubation), and Key Laboratory of Colleges and Universities in Hunan Province
for Cytobiology and Molecular Biotechnology, Hunan University of Chinese
Medicine, Changsha, Hunan 410208, China; Department of Medical Microbiology,
Immunology & Cell Biology, Simmons Cancer Institute, Southern Illinois University
School of Medicine, 913 N. Rutledge Street, Springfield, IL 62794, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20151228
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
SB  - IM
MH  - Animals
MH  - Colitis, Ulcerative/*complications/*pathology
MH  - Colorectal Neoplasms/*etiology/*pathology
MH  - DNA Damage
MH  - Humans
MH  - Models, Biological
MH  - *Oxidative Stress
MH  - *Protein Carbonylation
PMC - PMC4707327
OID - NLM: PMC4707327
EDAT- 2016/01/30 06:00
MHDA- 2016/12/15 06:00
CRDT- 2016/01/30 06:00
PHST- 2015/06/03 [received]
PHST- 2015/10/14 [revised]proliferation
PHST- 2015/10/25 [accepted]
AID - 10.1155/2016/9875298 [doi]
PST - ppublish
SO  - Oxid Med Cell Longev. 2016;2016:9875298. doi: 10.1155/2016/9875298. Epub 2015 Dec
28.
PMID- 22442342
OWN - NLM
STAT- MEDLINE
DA  - 20120608
DCOM- 20120817
LR  - 20130926
IS  - 1535-3699 (Electronic)
IS  - 1535-3699 (Linking)
VI  - 237
IP  - 5
DP  - 2012 May
TI  - Oxidative stress and redox signaling mechanisms of inflammatory bowel disease:
updated experimental and clinical evidence.
PG  - 4
74-80
LID - 10.1258/ebm.2011.011358 [doi]
AB  - Inflammatory bowel disease (IBD) comprises primarily the chronic relapsing
inflammatory disorders, Crohn's disease and ulcerative colitis, with the former
affecting any part of the gastrointestinal tract and the latter mainly afflicting
the colon. The precise etiology of IBD remains unclear, and it is thought that
interactions among various factors, including genetic factors, the host immune
system and environmental factors, cause disruption of intestinal homeostasis,
leading to dysregulated inflammatory responses of the gut. As inflammation is
intimately related to formation of reactive intermediates, including reactive
oxygen and nitrogen species (ROS/RNS), oxidative stress has been proposed as a
mechanism underlying the pathophysiology of IBD. This review is intended to
summarize succinctly recent new experimental and clinical evidence supporting
oxidative stress as a pathophysiological component of IBD and point to the
potential of using antioxidant compounds as promising therapeutic modalities of
human IBD. The sources of ROS/RNS and the redox signaling mechanism underlying
oxidative stress and inflammation in IBD are discussed to provide insight into
the molecular basis of oxidative stress as a pathophysiological factor in IBD.
FAU - Zhu, Hong
AU  - Zhu H
AD  - Laboratory of Molecular and Cellular Pharmacology and Toxicology, Department of
Pharmacology, EVCOM, Virginia Tech Corporate Research Center RBII, Blacksburg, VA
24060, USA. hzhu@vcom.vt.edu
FAU - Li, Y Robert
AU  - Li YR
LA  - eng
GR  - NIH DK81905/DK/NIDDK NIH HHS/United States
GR  - NIHHL93557/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20120322
PL  - England
TA  - Exp Biol Med (Maywood)
JT  - Experimental biology and medicine (Maywood, N.J.)
JID - 100973463
RN  - 0 (Reactive Nitrogen Species)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Animals
MH  - Colitis, Ulcerative/enzymology/genetics/*metabolism
MH  - Crohn Disease/enzymology/genetics/*metabolism
MH  - Humans
MH  - Inflammation
MH  - Mice
MH  - Oxidation-Reduction
MH  - *Oxidative Stress
MH  - Reactive Nitrogen Species/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - *Signal Transduction
MH  - Superoxide Dismutase/genetics/metabolism
EDAT- 2012/03/24 06:00
MHDA- 2012/08/18 06:00
CRDT- 2012/03/24 06:00
AID - ebm.2011.011358 [pii]
AID - 10.1258/ebm.2011.011358 [doi]
PST - ppublish
SO  - Exp Biol Med (Maywood). 2012 May;237(5):474-80. doi: 10.1258/ebm.2011.011358.
Epub 2012 Mar 22.
PMID- 22413852
OWN - NLM
STAT- MEDLINE
DA  - 20120524
DCOM- 20120926
LR  - 20120524
IS  - 1440-1746 (Electronic)
IS  - 0815-9319 (Linking)
VI  - 27
IP  - 6
DP  - 2012 Jun
TI  - Oxidative stress in inflammation-based gastrointestinal tract diseases:
challenges and opportunities.
PG  - 1004-10
LID - 10.1111/j.1440-1746.2012.07108.x [doi]
AB  - Oxygen free radicals in excessively high amounts are all very reactive chemically
and can impose a detrimental influence on living organisms by provoking
"oxidative stress" that can damage major cellular constituents. The latter
includes the cell membrane, cytoplasmic proteins, and nuclear DNA. Conversely,
nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS)
when present in low amounts play an important role as regulatory mediators in
signaling processes, through which, paradoxically, many ROS-mediated responses
can protect the cells against oxidative stress by induction of "redox
homeostasis." Therefore, diseases associated with free radical overproduction are
provoked by "blazed ROS productions" far beyond the host's capacity to quench.
Free radicals have been implicated in the pathogenesis of diverse
gastrointestinal (GI) diseases including gastroesophageal reflux disease (GERD),
gastritis, enteritis, colitis and associated cancers as well as pancreatitis and
liver cirrhosis. This article provides an overview of the role of oxidative
stress in inflammation-based GI tract diseases, including reflux esophagitis,
Helicobacter pylori-associated gastritis, non-steroidal anti-inflammatory
drug-induced enteritis, ulcerative colitis, and associated colorectal cancer. The
challenging issue that ROS can contribute to diverse gastrointestinal
dysfunction, or manifest dual roles in cancer promotion or cancer suppression
will also be discussed for the opportunity to enhance understanding of
inflammation-based GI diseases.
CI  - (c) 2012 Journal of Gastroenterology and Hepatology Foundation and Blackwell
Publishing Asia Pty Ltd.
FAU - Kim, Yoon Jae
AU  - Kim YJ
AD  - Department of Gastroenterology, Gachon University Gil Medical Center, Incheon,
Korea.
FAU - Kim, Eun-Hee
AU  - Kim EH
FAU - Hahm, Ki Baik
AU  - Hahm KB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Australia
TA  - J Gastroenterol Hepatol
JT  - Journal of gastroenterology and hepatology
JID - 8607909
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Cell Transformation, Neoplastic/metabolism
MH  - Gastroenteritis/complications/metabolism/*physiopathology
MH  - Gastrointestinal Neoplasms/etiology/physiopathology
MH  - Humans
MH  - Oxidative Stress/*physiology
MH  - Reactive Oxygen Species/metabolism
EDAT- 2012/03/15 06:00
MHDA- 2012/09/27 06:00
CRDT- 2012/03/15 06:00
AID - 10.1111/j.1440-1746.2012.07108.x [doi]
PST - ppublish
SO  - J Gastroenterol Hepatol. 2012 Jun;27(6):1004-10. doi:
10.1111/j.1440-1746.

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