Abstract
Aims: Effect of exogenously administered melatonin (N-acetyl 5-methoxytryptamine) on antioxidant systems in experimental Ischemia–Reperfusion (I-R) of rat gastrointestinal system (GIS) was examined.Methods: A total of 40 rats were divided into 4 groups: Group 1 (Sham), Group 2 (I-R), Group 3 (I-R + 10 mg/kg melatonin) and Group 4 (I-R + 20 mg/kg melatonin). Activity levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined in small intestines.Results: There was a significant (p<0.05) reduction in GSH-Px levels in Group 2 (64.16±7.02 U/mg protein) compared to Group 1 (80.15±9.32 U/mg protein). We observed a meaningful increase in GSH-Px levels in melatonin applied groups (Group 3: 75.94±9.83 U/mg protein, Group 4: 78.55±9.11 U/mg protein) compared to Group 2. Correspondingly, SOD activity levels were significantly reduced (p<0.001) in Group 2 (24.14±4.35 U/mg protein) compared to controls (52.91±6.13 U/mg protein). A stronger effect (p<0.001) of melatonin was observed on SOD levels compared to GSH-Px levels in both doses (Group 3: 38.96±6.39 U/mg protein, Group 4: 43.07±7.76 U/mg protein). Levels of selenium were reduced significantly in Group 2 (1.11±0.31 μg/g tissue) compared to Group 1 (2.01±0.19 μg/g tissue). Melatonin application in Group 3 (1.13±0.28 μg/g tissue) and Group 4 (1.89±0.48 μg/g tissue) caused an increase in selenium levels. There was a strong correlation between increases in selenium and GSH-Px levels in Group 4 (r:0.651 p<0.01).Conclusions: Melatonin seems to exert its antioxidant effect in GIS tract by stimulating SOD and GSH-Px. Selenium also seems to have an antioxidant contribution on protecting rat gastrointestinal tract I-R injury.
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