Kadir Özcan

Effectiveness of melatonin on aflatoxicosis in chicks.

The efficacy of melatonin co-administration on aflatoxicosis in chicks was investigated. Ross PM3 breed chicks were divided into groups of 10 and given conventional feed. One of the groups was kept as a control (C), and the others were given 150ppb aflatoxin (AF1), 300ppb aflatoxin (AF2), 150ppb aflatoxin plus 10mg/kg/bwt melatonin (AF1+M), 300ppb aflatoxin plus 10mg/kg/bwt melatonin (AF2+M), 10mg/kg/bwt melatonin (M), and 1% ethanol (E). After 21 day-treatment period, the chicks were sacrificed, liver and kidney tissues were collected, processed for immuno-histochemical staining, in situ TUNEL method, and biochemical analyses. Vacuolar degeneration, necrosis, bile duct hyperplasia in liver, and mild tubular degeneration in kidney were detected in AF groups. Pathological changes were markedly reduced in AF+M groups, and a microscopic view similar to group C was observed. Increased immunoreactivity against inducible nitric oxide synthase (iNOS) and nitrotyrosine was detected in AF groups compared to weak immunoreactivity in group C. Immunoreactivity in AF+M groups was markedly reduced compared to AF groups and was similar to group C in liver and kidney. Many apoptotic cells were detected in the livers of AF groups, whereas there were no apoptotic cells in AF+M groups. While reduced glutathione (GSH) levels in liver and kidney of AF groups were greatly reduced, malondialdehyde (MDA) levels increased. With melatonin co-administration, the levels of GSH and MDA approached to the values of group C. These results indicated that nitrosative tissue degeneration caused by aflatoxin could be greatly reduced by melatonin supplementation in chicks.

Pathological, biochemical and haematological investigations on the protective effect of α-lipoic acid in experimental aflatoxin toxicosis in chicks

1. The purpose of this study was to investigate the protective effect of α-lipoic acid (LA) on aflatoxin (AF) toxicosis in chicks. 2. Groups of 10 Ross PM3 chicks were given, for 21 d, no AF (C), 60 mg/kg/bwt of α-lipoic acid (LA), 150 ppb of aflatoxin (AF1), 150 ppb of aflatoxin plus 60 mg/kg/bwt of α-lipoic acid (AF1 + LA), 300 ppb of aflatoxin (AF2), and 300 ppb of aflatoxin plus 60 mg/kg/bwt of α-lipoic acid (AF2 + LA). Before the animals were killed, blood samples were drawn for haematological analysis, and then tissue samples were collected for histopathological investigation. Immunohistochemical staining was performed against inducible nitric oxide synthase (iNOS) and nitrotyrosine on liver samples. Apoptotic cell death in liver was assessed by in situ TUNEL assay. The malondialdehyde (MDA) and reduced glutathione (GSH) concentrayions in liver and kidney were also determined. 3. Hydropic degeneration and occasional necrosis, bile duct hyperplasia and periportal fibrosis were observed in the livers of AF-treated groups. The severity of these changes was reduced in LA-supplemented AF groups. Occasionally, thymic cortical atrophy, lymphoid depletion in spleen and bursa of Fabricius, and degeneration in the kidney tubule epitheliums were detected in AF groups. The severity of these degenerative changes was slightly reduced in LA supplemented groups. 4. There was moderate to strong iNOS and nitrotyrosine immunoreactivity in the livers of AF groups, while decreased immunoreactivity was observed against both antibodies in the LA supplemented groups. Apoptotic cells were numerous in the AF groups, while greatly reduced in LA supplemented groups. 5. In the liver and kidney of AF-treated groups given 300 ppb of aflatoxin, MDA concentrations were increased as GSH decreased, compared to the control group. LA supplementation of AF-treated birds improved the results compared to the AF only groups, however a statistical difference was observed only in liver tissues between AF2 + LA and AF2 groups. Haematological variables showed no differences among the groups. 6. In conclusion, supplementation of feed with the antioxidant LA, might ameliorate the degenerative effects caused by aflatoxin due to lipid peroxidation.

Histopathologic, biochemical and genotoxic investigations on chronic sodium nitrite toxicity in mice.

The aim of this study was to investigate the effects of long term Sodium nitrite (NaNO2) consumption. Swiss albino mice were given NaNO2 (0, 10 and 20 mg/kg/day) as mixed in feed for 8 months. At the end of treatments, animals were sacrificed and selected organs were processed for histopathologic, imunohistochemical, biochemical and genotoxic investigations. Mild to moderate degenerative changes were observed in liver, kidney, intestine, lung and spleen of NaNO2-given mice. Inducible nitric oxide synthase and nitrotyrosine activities increased in liver and kidney of NaNO2-given mice. Proliferating cell nuclear antigen activity increased in liver. Apoptotic cell death was observed in livers of the treatment groups. Liver malondialdehyde level was higher in the treatment groups while no change was seen in kidney. Nitric oxide levels in both liver and kidney of the treatment groups were lower than those of the control group. In genotoxic investigations, the number of chromosome and chromatid breaks, chromatid association, and polyploidy increased while mitotic index decreased in NaNO2-given mice. The results showed that NaNO2 would cause histopathologic changes, nitrosative tissue damage, and lipid peroxidation in liver and kidney, as well as induce chromosomal aberrations even if it was given at low levels for long time.

Diprosopus, craniorachischisis, arthrogryposis, and other associated anomalies in a stillborn lamb

Congenital malformations with multiple anomalies have been described infrequently in the veterinary literature. A stillborn male crossbred lamb with diprosopus, craniorachischisis, and arthrogryposis was examined macroscopically and histopathologically in this study. The left head was smaller than the right head. Micrencephaly, agnathia, and a rudimentary tongue, which was adherent to the palate, were present in the left head. Micrencephaly, brachygnathia superior, and cleft palate were present in the right head. Cerebellar agenesis and spinal cord hypoplasia were observed. The cerebrums and the spinal cord were covered with a tapering membranous structure. Neural and dermal tissues were noted to intervene upon microscopic examination of this structure. Disorganization of neurons was observed in both cerebrums, though it was more severe in the left one. This case demonstrates many congenital defects occurring together in a lamb.

Occurrence of Helicobacter Infection in the Gastric Mucosa of Free-living Red Foxes (Vulpes vulpes)

We studied gastric Helicobacter spp. in five red foxes (Vulpes vulpes). Samples of stomach from the cardia, corpus, pyloric antrum, and duodenum were subjected to histopathologic, immunohistochemical, and transmission electron microscopy (TEM) examination for the presence of Helicobacter and gastritis. All foxes had gastric Helicobacter-like organisms (GHLOs) on examination by light microscopy and TEM. Gastric Helicobacter-like organisms were present in all areas of the stomachs. Chronic mild or moderate gastric inflammation was associated with infection by GHLOs in one or more regions of the stomach, but there was no correlation between inflammation and infection. It is not clear whether the organisms were causing the minimal histologic lesions observed, but the gastric mucosa of free-living foxes appears to be commonly colonized with GHLOs. The frequent colonization of free-living foxes with distinct GHLOs possibly reflects their special characteristic in feeding and/or social behavior or the potential commensal nature of the bacteria in free-ranging foxes.