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.