Loss of manganese superoxide dismutase expression and activity in rat esophagus with external esophageal perfusion

Yan Li, John Wo, Ruifeng R. Su, Mukunda B. Ray, Robert C G Martin

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Background: Manganese superoxide dismutase (MnSOD), the primary antioxidant enzyme that scavenges superoxide radicals found in the mitochondria, has been shown to protect oxygen-utilizing cells from the toxicity of the reactive oxygen species (ROS). Current studies in the animal esophageal reflux model are limited, and the reports on the relevance of protein expression level and enzymatic antioxidative activity of MnSOD in esophageal mucosal defense are controversial. Thus, the aim of this study is to investigate the role of MnSOD expression and activity in rats with esophageal perfusion injury. Methods: We have established a novel external esophageal perfusion (EEP) animal model that allows for esophageal reflux injury. We used the model with 0.5% bovine bile as the perfusion agent in one group of rats and used saline in another group to serve as controls. The esophageal mucosal was isolated for MnSOD expression and activity analysis. Results: Severe esophagitis was observed in the mucosa at 1, 2, and 4 week(s) after bile perfusion. A significant decrease in MnSOD expression with bile perfusion was demonstrated by Western blotting and immunohistochemical evaluation. Similarly, a reduction in MnSOD enzyme activity was observed in bile-perfused rats compared with the saline-perfused controls; no decrease in copper/zinc SOD enzyme activity was observed. Conclusions: MnSOD expression and activity is decreased in bile-induced esophagitis. This decrease in MnSOD expression and activity is associated with esophagitis and cell death. This study suggests that the loss of MnSOD protein contributes to the reduced level of its enzymatic activity and plays a key role in the induction of esophagitis.

Original languageEnglish (US)
Pages (from-to)359-367
Number of pages9
JournalSurgery
Volume141
Issue number3
DOIs
StatePublished - Mar 2007
Externally publishedYes

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Esophagus
Superoxide Dismutase
Perfusion
Bile
Esophagitis
Gastroesophageal Reflux
Enzymes
Wounds and Injuries
Superoxides
Zinc
Copper
Reactive Oxygen Species
Mitochondria
Mucous Membrane
Proteins
Cell Death
Animal Models
Antioxidants
Western Blotting
Oxygen

ASJC Scopus subject areas

  • Surgery

Cite this

Loss of manganese superoxide dismutase expression and activity in rat esophagus with external esophageal perfusion. / Li, Yan; Wo, John; Su, Ruifeng R.; Ray, Mukunda B.; Martin, Robert C G.

In: Surgery, Vol. 141, No. 3, 03.2007, p. 359-367.

Research output: Contribution to journalArticle

Li, Yan ; Wo, John ; Su, Ruifeng R. ; Ray, Mukunda B. ; Martin, Robert C G. / Loss of manganese superoxide dismutase expression and activity in rat esophagus with external esophageal perfusion. In: Surgery. 2007 ; Vol. 141, No. 3. pp. 359-367.
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abstract = "Background: Manganese superoxide dismutase (MnSOD), the primary antioxidant enzyme that scavenges superoxide radicals found in the mitochondria, has been shown to protect oxygen-utilizing cells from the toxicity of the reactive oxygen species (ROS). Current studies in the animal esophageal reflux model are limited, and the reports on the relevance of protein expression level and enzymatic antioxidative activity of MnSOD in esophageal mucosal defense are controversial. Thus, the aim of this study is to investigate the role of MnSOD expression and activity in rats with esophageal perfusion injury. Methods: We have established a novel external esophageal perfusion (EEP) animal model that allows for esophageal reflux injury. We used the model with 0.5{\%} bovine bile as the perfusion agent in one group of rats and used saline in another group to serve as controls. The esophageal mucosal was isolated for MnSOD expression and activity analysis. Results: Severe esophagitis was observed in the mucosa at 1, 2, and 4 week(s) after bile perfusion. A significant decrease in MnSOD expression with bile perfusion was demonstrated by Western blotting and immunohistochemical evaluation. Similarly, a reduction in MnSOD enzyme activity was observed in bile-perfused rats compared with the saline-perfused controls; no decrease in copper/zinc SOD enzyme activity was observed. Conclusions: MnSOD expression and activity is decreased in bile-induced esophagitis. This decrease in MnSOD expression and activity is associated with esophagitis and cell death. This study suggests that the loss of MnSOD protein contributes to the reduced level of its enzymatic activity and plays a key role in the induction of esophagitis.",
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