No abstract

Free radicals are thought to be the most important cause of the reperfusion injury subsequent to ischemia. The antioxidant status of the tissue affected by ischemia-reperfusion is of great importance for the primary endogenous defense against the free radical induced injury. This investigation was performed to evaluate the antioxidant enzyme capacity of the brain tissue in the ischemia-reperfusion period using an experimental global moderate (penumbral) ischemia model on rat brains. Experiments were performed on 45 male Sprague Dawley rats. Ischemia was induced by bilateral vertebral arteries cauterization and temporary bilateral carotid arteries occlusion and sustained for 10 minutes. At the end of ischemia (0 min reperfusion) and various reperfusion periods (20 min, 60 min, 240 min), rats were decapitated and brains were frozen in liquid nitrogen. Changes in the intracellular antioxidant enzyme (superoxide dismutase, glutathione peroxidase and catalase) activities were assessed in the rat brain tissues, by spectrophotometric methods. In all moderate ischemia-reperfusion groups, superoxide dismutase activities were found to have decreased significantly compared to the sham operated controls (P < 0.05). During ischemia superoxide dismutase activity was lowered to 31% of that of the control group. The decreases were more significant in reperfusion groups, particularly in 60 min reperfusion (40%). Relatively smaller but still significant diminution was observed in glutathione peroxidase activities (P < 0.05). The ratio of diminution was striking in 20 min and 60 min reperfusion groups with 26% of the sham operated rats. Conversely, moderate ischemia-reperfusion caused significant increase in catalase activities (P < 0.05). The increment was 63% of the preischemic level with 10 min of moderate ischemia. In conclusion, activities of the major antioxidant enzymes were changed significantly in moderate brain ischemia-reperfusion. These results suggest that the disturbance in oxidant-antioxidant balance might play a part in rendering the tissue more vulnerable to free radical induced injuries.

The balance between matrix metalloproteinases (MMPs) and their physiological tissue inhibitors of matrix metalloproteinases (TIMPs) is crucial in tumour invasion and progression. The aim of this study was to investigate the levels of MMP-9, MMP-3 and TIMP-1 in colorectal cancer (CRC) and to evaluate these proteinases and their inhibitor with respect to clinicopathological variables. Activities of pro- and active MMP-9 were measured in paired tumour and distant normal tissue specimens from 43 patients with CRC using gelatin zymography. ELISA was employed for the determination of MMP-9, MMP-3 and TIMP-1 protein expressions. The activity levels of pro- and active MMP-9 and protein expression levels of MMP-9, MMP-3 and TIMP-1 were higher in tumour tissues than in the corresponding normal tissues; the differences being significant for all (p < 0.05), except TIMP-1. Similarly, active MMP-9/proMMP-9 and the ratio of protein expression level of MMP-9-TIMP-1 were found to be significantly higher in tumour tissues ( p < 0.01). Among all the clinicopathological variables investigated, significant correlations were found between MMP-9 and presence of perineural invasion, MMP-3 and lymph node status, TIMP-1 and tumour differentiation, MMP-9/TIMP-1 ratio and histological types ( p < 0.05). In conclusion, MMP-3 was not as notably increased as MMP-9 in tumour tissues. However, different roles may be attributed to MMP-9 and MMP-3 in CRC development and progression. Additionally, assessment of TIMP-1 in relation to MMPs appeared to be crucial in CRC studies to provide a basis for the re-evaluation of the clinical usefulness of TIMP-1 in colorectal cancer.

Study design: An experimental study examining the neuroprotective eect of magnesium on axonal function and lipid peroxidation in a rat model of acute traumatic spinal cord injury. Objective: To determine the eectiveness of postinjury treatment with magnesium on evoked potentials and lipid peroxidation after spinal cord injury (SCI). Setting: Pamukkale University, Denizli, Turkey. Methods: Spinal cord injury occurred in 30 rats with an aneurysm clip at T9 and the rats were randomly assigned to undergo subcutaneous administration of one of the following at 1 h after injury: (1) Physiological saline (n=10); (2) MgSO 4 , 300 mg/kg (n=10) and (3) MgSO 4 , 600 mg/kg (n=10). Spinal somatosensory evoked potentials (SSEPs) were recorded before injury, 30 min after injury and 3 h after injections. Rats were killed 24 h after the injury, and malondialdehyde (MDA) levels were measured. Results: Following SCI, there were signi®cant decreases in the amplitudes of P1 and N1 (P50.001) and only high-dose magnesium improved the SSEPs (P50.01). On the other hand, there was signi®cant dierence in lipid peroxide content between high-dose magnesium treated group and both of saline treated and low-dose magnesium treated groups (P50.01). Conclusion: These results suggest that magnesium has a dose-dependent neuroprotective eect on SSEPs and lipid peroxidation after experimental spinal cord injury.

ABSTRACT:Maternal milk plays an important role in breast milk jaundice (BMJ) development and is the major source of epidermal growth factor (EGF) for neonates. The aim of this study was to investigate whether there is a relationship between EGF levels in the infant serum and in the milk of nursing mothers and BMJ. Two groups were defined: study group (n ϭ 30), newborns who were followed up for BMJ without any identifiable pathologic cause; control group, healthy newborns whose serum total bilirubin levels were Ͻ10 mg/dL. Milk and infant plasma samples were collected between the third and the fourth postpartum week. EGF concentrations in all of the samples were determined by using ELISA. The infants with BMJ had higher concentrations of EGF in the serum and in the breast milk compared with that of the infants without BMJ. The milk concentrations of EGF were significantly correlated with neonatal bilirubin and blood EGF concentrations. The degree of BMJ was associated with the increased levels of milk borne EGF. Although the exact mechanisms of the hyperbilirubinemic action of EGF are not completely known, the inhibition of gastric motility, increased absorption, and activation of bilirubin transport have been suggested as possible mechanisms. (Pediatr Res 66: 218-221, 2009) L ate onset breast milk jaundice (BMJ), also called BMJ syndrome, after the fifth day, a majority of breastfed infants either maintain a stable, but elevated serum bilirubin level, or have a second rise in bilirubin, which generally peaks on approximately 10th to 15th days of life. In some infants, these elevated levels may continue for many weeks, whereas in others, the levels decline during the third and fourth weeks. During the third week of life, among the two thirds or more with elevated levels, 2 to 4% of infants have a bilirubin level Ͼ10 mg/dL (170 mM) at 3 wks of age. Rarely do the levels in healthy term infants rise beyond 25 mg/dL (425 mM) or place the infant at risk for bilirubin encephalopathy. Ultimately, serum bilirubin levels return to normal in all infants with BMJ. Persistence of hyperbilirubinemia beyond 3 mo would suggest an etiology other than breast milk. The jaundice of breastfed infants is commonly of undetermined etiology (1-11). As reviewed elsewhere (12), many pathophysiologic theories have arisen to explain this prolonged nonconjugated hyperbilirubinemia associated with human milk feedings in otherwise healthy infants. The most attractive and convincing evidence regarding the mechanism of BMJ has come from studies of the effect of human milk on the intestinal absorption of bilirubin with resultant increase in enterohepatic circulation of bilirubin. Milk from mothers of infants with classical BMJ inhibited intestinal absorption of bilirubin only for the first 2 h and was then followed by a dramatic increase in absorption, which continued for at least an additional 14 h and resulted in a total absorption of 60% of the intestinal bilirubin dose. A subsequent study by other investigators confirmed the role of human milk...