Protective effect of melatonin on antioxidative system in experimental ischemia-reperfusion of rat small intestine

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.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&lt;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&lt;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&lt;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 microg/g tissue) compared to Group 1 (2.01+/-0.19 microg/g tissue). Melatonin application in Group 3 (1.13+/-0.28 microg/g tissue) and Group 4 (1.89+/-0.48 microg/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&lt;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.</p

Hemochromatosis Presenting with Ascites in a Newborn Infant

Background: Although the incidence of neonatal hemochromatosis (NH) is not known exactly, it is one of the causes of acute liver failure in the newborns. NH is a rare iron metabolism disease characterized by excessive iron accumulation in the tissues that onsets in-utero. Here, a patient diagnosed with NH who developed ascites while investigating the etiology of cholestasis has been presented. Case report: A 35-week-old premature female baby was referred us to investigate the etiology of cholestasis. She had a sibling who died at 34 days of age due to liver failure. Abdominal examination revealed a palpable liver 4 cm from the costal margin. On laboratory, aspartate transaminase was 111 U/L (range 9-80), alanine transaminase 62 U/L (range 8-32), total bilirubin 12.6 mg/dL, and direct bilirubin 5 mg/dL. Prothrombin time was 18.4 sec (range 10-14) and INR 1.86 (range 0.8-1.2). Magnetic resonance imaging revealed a diffuse reduction in liver density due to iron accumulation. Focal iron accumulation consistent with NH was observed in hepatocytes in liver biopsy. In the clinical follow-up, the patient developed abdominal distension. Abdominal ultrasonography showed excessive fluid accumulation in the abdominal cavity. Following intravenous immunoglobulin (1g/kg, single dose) and antioxidant cocktail, her abdominal distension subsided and liver function tests regressed. The patient has been discharged on the postnatal 67th day with planned liver transplantation. Conclusion: Neonatal hemochromatosis should definitely be kept in mind in newborns with hepatic failure. As seen in this case, NH should also be considered in the differential diagnosis of ascites in newborn infants