The study aimed at determining the effect of melatonin on the activity of protective antioxidative enzymes in the heart and of lipid peroxidation products in the course of intoxication with doxorubicin (DOX). The rats were categorized into four groups, receiving: 0.9% NaCl i.p. (NaCl control); melatonin [20 mg/kg body weight (b.w.)] s.c. (control Mel); DOX (2.5 mg/kg b.w.) i.p.; melatonin plus DOX in doses as above. All the substances were administered once in a week for four consecutive weeks. Homogenates of heart tissue were examined for activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), levels of reduced glutathione (GSH) and of lipid peroxidation indices (MDA + 4-HDA). Administration of melatonin alone did not induce alterations in levels of MDA + 4-HDA, GSH, or in activity of GPx, SOD or CAT, as compared to the group receiving 0.9% NaCl. GSH levels decreased following DOX but remained at normal levels following DOX and melatonin. The level of MDA + 4-HDA increased following DOX, as compared with the control, a change prevented by the combination of DOX + melatonin. Activities of GPx, SOD and CAT were higher in groups receiving DOX and/or DOX plus melatonin than in control groups. Activity of CAT and the level of GSH in the group receiving DOX plus melatonin were significantly higher than in the group intoxicated with DOX alone. The obtained results demonstrate that, when given in parallel with DOX, melatonin protects cardiomyocytes from damaging effects of the cytostatic drug (reflected by the levels of MDA + 4-HDA). The protective effect resulted, in part from the augmented levels of GSH and from stimulation of CAT activity by melatonin in cardiomyocytes subjected to the action of DOX.

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The data presented herein strongly point out the importance of the immunological and morphological injury that occurs before and during transplantation. The increase of inflammatory response after brain death is important for further stimulation of the immune response and long-term kidney survival.

Human colon Cancer usually develops on a mucosa which has already undergone multiple steps of genetic change. These multiple steps create a field effect characterized by the presence of morphologically normal, but biologically altered epithelial cells. This aims of this study were to evaluate whether the expression of carcinoembryonic antigen (CEA) can act as a phenotypic marker of the field effect, and to map its topography in relation to the presence of colorectal adenocarcinoma. The expression of CEA was tested by immunohistochemistry on morphologically normal mucosa at 4 increasing distances from 14 autologous cases of colorectal adenocarcinoma. CEA expression in the normal mucosa was compared to the tumor. The results show that in the mucosa adjacent to the edge of the autologous tumor, CEA is expressed to the same level as displayed in the Carcinoma; there is a decrease in CEA expression in normal mucosa located at 1 cm or more from the edge of Carcinoma. Mucosa sampled at 5 and 10 cm from the tumor expresses CEA at the same low level as in mucosa of control subjects with no colorectal neoplasm. In conclusion, this study demonstrates a gradient of CEA expression in the peritumoral area, supporting the concept of field effect, and maps its extent. These data are relevant to the biology of human colorectal Cancer, and more practically, to the optimal location of surgical resection.