Abstract
Over the past several years, there has been increasing recognition that pathogenesis of adhesion development includes significant contributions of hypoxia induced at the site of surgery, the resulting oxidative stress, and the subsequent free radical production. Mitochondrial dysfunction generated by surgically induced tissue hypoxia and inflammation can lead to the production of reactive oxygen and nitrogen species as well as antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase which when optimal have the potential to abrogate mitochondrial dysfunction and oxidative stress, preventing the cascade of events leading to the development of adhesions in injured peritoneum. There is a significant cross talk between the several processes leading to whether or not adhesions would eventually develop. Several of these processes present avenues for the development of measures that can help in abrogating adhesion formation or reformation after intraabdominal surgery.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 823-836 |
| Number of pages | 14 |
| Journal | Reproductive Sciences |
| Volume | 21 |
| Issue number | 7 |
| DOIs | |
| State | Published - Jan 1 2014 |
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Keywords
- adhesion markers
- hypoxia
- oxidative stress
- postoperative adhesions
ASJC Scopus subject areas
- Obstetrics and Gynecology
Cite this
Advances in the pathogenesis of adhesion development : The role of oxidative stress. / Awonuga, Awoniyi O.; Belotte, Jimmy; Abuanzeh, Suleiman; Fletcher, Nicole M.; Diamond, Michael Peter; Saed, Ghassan M.
In: Reproductive Sciences, Vol. 21, No. 7, 01.01.2014, p. 823-836.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Advances in the pathogenesis of adhesion development
T2 - The role of oxidative stress
AU - Awonuga, Awoniyi O.
AU - Belotte, Jimmy
AU - Abuanzeh, Suleiman
AU - Fletcher, Nicole M.
AU - Diamond, Michael Peter
AU - Saed, Ghassan M.
PY - 2014/1/1
Y1 - 2014/1/1
N2 - Over the past several years, there has been increasing recognition that pathogenesis of adhesion development includes significant contributions of hypoxia induced at the site of surgery, the resulting oxidative stress, and the subsequent free radical production. Mitochondrial dysfunction generated by surgically induced tissue hypoxia and inflammation can lead to the production of reactive oxygen and nitrogen species as well as antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase which when optimal have the potential to abrogate mitochondrial dysfunction and oxidative stress, preventing the cascade of events leading to the development of adhesions in injured peritoneum. There is a significant cross talk between the several processes leading to whether or not adhesions would eventually develop. Several of these processes present avenues for the development of measures that can help in abrogating adhesion formation or reformation after intraabdominal surgery.
AB - Over the past several years, there has been increasing recognition that pathogenesis of adhesion development includes significant contributions of hypoxia induced at the site of surgery, the resulting oxidative stress, and the subsequent free radical production. Mitochondrial dysfunction generated by surgically induced tissue hypoxia and inflammation can lead to the production of reactive oxygen and nitrogen species as well as antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase which when optimal have the potential to abrogate mitochondrial dysfunction and oxidative stress, preventing the cascade of events leading to the development of adhesions in injured peritoneum. There is a significant cross talk between the several processes leading to whether or not adhesions would eventually develop. Several of these processes present avenues for the development of measures that can help in abrogating adhesion formation or reformation after intraabdominal surgery.
KW - adhesion markers
KW - hypoxia
KW - oxidative stress
KW - postoperative adhesions
UR - http://www.scopus.com/inward/record.url?scp=84904625770&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84904625770&partnerID=8YFLogxK
U2 - 10.1177/1933719114522550
DO - 10.1177/1933719114522550
M3 - Review article
VL - 21
SP - 823
EP - 836
JO - Reproductive Sciences
JF - Reproductive Sciences
SN - 1933-7191
IS - 7
ER -