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Number of results: 4
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Abstract

The present study was undertaken to highlight the influence of simvastatin administration on hepatocyte morphology, proliferation, and apoptosis. The study included 48 gilts aged 3 months (weighing ca. 30 kg) divided into groups I (control; n=24) and II, receiving 40 mg/animal simvas- tatin orally (simavastatin; n=24) for 29 days. The animals were euthanized on days subsequent to the experiment. The livers were sampled, fixed, and processed routinely for histopathology, histochemistry, and immunohistochemistry (for proliferating cell nuclear antigen, Bcl-2, and caspase-3). Apoptosis was visualized by terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL). Simvastatin administration caused acute hepatocyte swelling, glycogen de- pletion, hyperaemia, multifocal hepatocyte proliferation with occasional pseudoacinar formation, connective tissue hyperplasia, eosinophil infiltration, and interface hepatitis. The proliferating cell nuclear antigen index, mean diameter of argyrophilic nucleolar organizer regions, and Bcl-2 immunoexpression were lower compared to control, and mean caspase-3 immunoexpression was higher in group II compared to control. On day 25 and 29 single hepatocytes in the simvasta- tin-treated group were TUNEL-positive. Simvastatin caused morphological alteration which became more intense over time. The results from the present study suggest that simvastatin treat- ment may cause glycogen, lipid metabolism and cell membrane permeability distortion, fibrosis, interface hepatitis, reduction in hepatocyte proliferation and transcriptional activity, and enhanced vulnerability to apoptosis. Summing up the results, it can be concluded that simvastatin caused liver damage with similar morphological changes seen in autoimmune-like liver injury, which may indicate that simvastatin may induce autoimmune-like drug induced liver injury.
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Abstract

The present study was aimed to investigate oxidative stress, DNA damage, and histopatholog- ical alterations in hepatic tissues of splenectomized Wistar rats experimentally infected with Ba- besia bigemina. Rats were challenged with 5x106 infected erythrocytes. Babesia infection was con- firmed both with Giemsa’s staining blood smears and nested-PCR amplified region of apical membrane antigen-1 (AMA-1) gene. Parasitemia reached approximately 10 % at day 5 post-in- fection. Livers of infected rats were enlarged and darker in color, became extremely brittle with marked congestion. Microscopic evaluation showed cytoplasmic clearing of hepatocytes and se- vere hydropic changes with significantly dilated sinusoids containing macrophages and also intra- sinosoidal parasitized erythrocytes. Severe infiltration of lymphoplasma cells was also present throughout the liver parenchyma. Furthermore, Kupffer cells were enlarged and, occasionally, containing Babesia-parasitized erythrocytes. The activity of Glutathione (GSH) and catalase (CAT), and total antioxidant capacity (TAC) were also significantly decreased (p < 0.05) after infection of rats with B. bigemina. B. bigemina infection also induced a significant increase (p < 0.05) in hepatic malondialdehyde (MDA) and nitric oxide-derived products (NOx) concentra- tions as well as amount of endogenous hepatocytes DNA damage. Hepatic damage was also re- flected through the measurement of lactic acid dehydrogenase (LDH) and protein carbonyl con- tent (PCO) in liver cells. These two indices of liver injury were also significantly elevated (p < 0.5) during B. bigemina infection. Evaluation of correlation between assayed variables in infected rats revealed that MDA levels were positively correlated with PCO, NOx, LDH and DNA damage in the infected group and negatively correlated with GSH, CAT and TAC. There was also an inverse relationship between the antioxidant enzymes activities of GSH, CAT and TAC with PCO, NOx and DNA damage in infected rats. However, NOx showed positive correlation with PCO and DNA damage in infected rats. On the basis of the above results it can be concluded that the Ba- besia infection increases oxidative stress markers, protein carbonyl content and DNA damage and decreases antioxidant enzymes activities in the liver. These results suggest that B. bigemina infec- tion could alter the liver histopathology and causes DNA damage following oxidative stress in hepatic tissue. Further studies are needed to precisely define how hepatic tissue damage takes place in B. bigemina infection.
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Abstract

The aim of this study was to verify the hypothesis postulating that the supplementation of turkey diets with Cu nanoparticles can lower dietary inclusion levels of Cu without compromising the growth rate and antioxidant status of turkeys. The experiment was carried out on 648 one-day-old Hybrid Converter turkeys divided into 6 groups with 6 replicates per group, in a two-factorial design with 3 dietary inclusion levels of Cu (20, 10 and 2 mg/kg) and 2 dietary sources of Cu - copper sulfate (Cu-SUL) and Cu nanoparticles (Cu-NP). At 42 days of age, blood samples were collected from 2 birds per replicate (12 birds per group), after slaughter livers were collected for analyses. Blood and liver samples were assayed for: Cu, Zn, Ca, P, Mg, GLU, TP, ALB, UREA, TAG, TC, UA, ALT, AST, ALT, GGT, ALP, SOD, GPx, CAT, VIT C, FRAP, GSH+GSSG, LOOH, MDA. The results of this experiment demonstrate that a decrease in the dietary inclusion levels of Cu from 10 mg/kg to 2 mg/kg does not compromise the growth performance of turkeys, but weakens antioxidant defense mechanisms. A Cu dose of 20 mg/kg induces oxidation reactions and has a much more inhibitory effect on the antioxidant defense system than dietary Cu content of 2 mg/kg. In turkeys, dietary supplementation with Cu-NP has a more beneficial effect on carbohydrate metabolism and antioxidant status compared with Cu-SUL. The results of analyses examining the antioxidant and metabolic status of young turkeys indicate that 10 mg/kg is the optimal dietary inclusion level of Cu.
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Abstract

Lipogranulomas are lesions found in histopathological liver examination in humans and in various animal species, including dogs, especially those with portosystemic shunts. They consist of macrophages and other inflammatory cells, and sometimes they contain iron salts (pigment granuloma). This study aimed at determining the number of granulomas and cellular composition of lipogranulomas in dogs with the congenital extrahepatic portosystemic shunt, and to identify factors associated with their development. 44 archival liver samples from dogs with portosystemic shunt were stained using HE, Perl’s method and – in randomly-selected cases – immunohistochemically against CD56, CD20 and CD3 (DAKO). A reduction in the size of the liver was observed in all dogs during laparotomy, and the diameter of the vessel circumventing the liver was also measured (in 24 dogs). Lipogranulomas were found in 52.3% of samples; iron salts were present in 47.8% of them; 72% of cells in lipogranulomas were macrophages. In lipogranulomas both types of lymphocytes – T and B – were seen. The presence of lipogranulomas in liver samples in dogs was connected with fatty degeneration of hepatocytes and was correlated with the age of animals and with the diameter of the abnormal vessel circumventing the liver. Their formation appears to be triggered by severe ischemia and shortage of nutrient supply.
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