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ABSTRACT Two different neoplasms in the same biopsy material, called collision tumour, were studied. These tumours are rarely seen in the skin. We report the case of a 79-year-old female with a collision tumour composed of amelanotic malignant melanoma and atypical fibroxanthoma of the face. The histological and immunopathological features observed are discussed.
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ABSTRACT Objective: Ethyl alcohol (EA) is a substance that is used commonly worldwide and known to have toxic effects on the liver. The aim of this study was to investigate the effect of montelukast sodium (MK) on acute hepatopathy induced by a single dose of EA in rats. Methods: The study consisted of four groups each containing eight Wistar albino male rats. The groups were classified as follows: the control group received distilled water; the EA group received 6 g/kg EA diluted with distilled water orally by gavage; the MK group received 30 mg/kg MK orally by gavage; the EA + MK group received, 2 hours after the EA administration, ie 30 mg/kg MK orally by gavage. After 24 hours, all the rats were sacrificed, and their blood and liver tissue samples were taken for biochemical and histopathological examinations. Results: The administration of EA caused a statistically significant increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels compared with the control group (220.50 ± 66.90 and 92.38 ± 5.90 versus 84.88 ± 15.66 and 43.75 ± 10.22). The administration of EA + MK caused a statistically significant decrease in the AST and ALT levels compared with the EA alone group. Ethyl alcohol administered to the rats caused lesion in the liver including congestions, hydropic degeneration and irregular shaped area caused coagulation necrosis. The histopathological changes seen in the EA group were not detected in the EA + MK group. Conclusion: Consequently, these data suggested that MK had beneficial effects in alleviating EA-induced hepatotoxicity in rats.
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ABSTRACT Objective: To investigate the protective effects of caffeic acid phenethyl ester (CAPE) against isoniazid (INH)- and rifampicin (RFP)-induced hepatic and pancreatic damage. Methods: Eighty adult rats were randomly divided into eight groups: control, INH, RFP, INH+RFP, INH+CAPE, RFP+CAPE, INH+RFP+CAPE, and CAPE. Both INH and RFP were orally administered for 30 days at a dose of 50 mg/kg/day. Caffeic acid phenethyl ester was intraperitoneally injected for 30 days (10 μmol/kg). Blood samples, hepatic and pancreatic tissues were obtained on day 30. Results: Total oxidant status levels were significantly higher in INH and/or RFP-treated groups than those of control and CAPE groups, while total antioxidant status and paraoxonase levels were significantly reduced in INH-RFP groups compared with the group receiving CAPE. Histopathological deterioration was observed in RFP and INH groups in pancreatic and hepatic tissue. However, significant amelioration was observed in CAPE-treated groups. Conclusion: Our findings suggest that CAPE may be a promising agent to prevent the side effects of INH and RFP treatment on hepatic and pancreatic tissues.
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OBJECTIVE: Ethyl alcohol is a substance that is widely used worldwide and known to exert toxic effects on liver. In this study, we aimed to examine the effect of L-ornithine L-aspartate (LOLA) on the toxicity of a single dose of ethyl alcohol in rats. SUBJECTS AND METHOD: We used 32 randomly selected male Sprague-Dawley rats weighing 200-250 g. The rats were grouped into four groups with each group containing eight rats: Group 1: the control group, Group 2: the ethyl alcohol group, Group 3: the LOLA group and Group 4: the ethyl alcohol+LOLA group. Ethyl alcohol was administered orally through a nasogastric tube at a dose of 6 g/kg after diluting with distilled water. One hour after ethyl alcohol administration, LOLA was administered to pre-specified groups orally through a nasogastric tube at a dose of 200 mg/kg after diluting with distilled water. Liver tissue and blood samples were obtained from all rats 24 hours later to study total antioxidant capacity (TAC), total oxidant status (TOS) and oxidative stress index (OSI) levels in liver samples, and aspartate aminotransferase (AST), alanine transferase (ALT), TAC, TOS and OSI levels in blood samples. RESULTS: Serum TAC, TOS and OSI levels were higher in the groups that were administered ethyl alcohol. In addition, tissue TAC level was higher and TOS and OSI levels were lower in groups that were given ethyl alcohol. No significant changes were observed in serum and tissue TAC, TOS, OSI, ALT and AST levels in the LOLA administered groups. CONCLUSION: This study showed that LOLA was not biochemically effective and exerts no oxidative stress reducing activity in liver injury due to acute ethyl alcohol toxicity.