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Background. Since arsenic compounds have an affinity to thiol groups their greatest amounts can then be found in the tissues containing sulphur - rich proteins, like beta- keratin in skin, hair and nails. Accumulation of arsenic also depends on the macronutrient content in daily food ration. The deficiency and excess of both the protein and fat may contribute to a higher content of arsenic in the organism, including hair in human or fur in animals. Objective. Hair and fur is a good indicator of population exposure to many toxic substances, including arsenic. The degree of arsenic accumulation may depend on the diet and nutritional status. The aim of this study was to determine the effect of protein and fat in diet on the accumulation of arsenic in rats’ fur. Material and Methods. A total number of 70 male Buffalo rats (body weight 200 - 220 g, age - 6 weeks) were divided into 10 groups. Rats were housed in plastic cages (4 per cage) in a 12h light/dark cycle for 6 weeks. The diets of different protein and fat contents ware administered to the animals. Five of ten groups of rats received throughout the whole period 10 ppm sodium arsenite dissolved in distilled drinking water (about 250 μg As/animal/day). The arsenic were determined with the method of atomic adsorption spectrometry in conjunction with a graphite-furnace atomize using a Varian AA240FS apparatus. Results. The highest arsenic concentrations were found in fur of rats which were given low protein diet and water with arsenic. The lowest arsenic contents were found in fur of rats, which were given control diet and high protein diet with arsenic in water. Conclusions. Balanced control diet or high protein diet protected organism from arsenic accumulation, only small increase of arsenic content in rats’ fur, compared to the control group, was observed.
W swojej pracy autor przedstawia kluczowe aspekty związane z chorobami oczu występującymi u kotów, które  powoduje  herpesvirus  koci typu 1. Praca  w obszerny sposób omawia wiele chorób implikowanych tym typem wirusa. szczegółowo opisuje objawy kliniczne poszczególnych schorzeń, diagnostykę oraz doradza w sposób praktyczny dobieranie odpowiedniego leczenia. Mamy podany szereg leków wraz z dawkami i sposobami ich podania dla poszczególnych schematów leczenia. Praca jest bogato ilustrowana fotografiami obrazującymi konkretne przypadki kliniczne. Autor włożył wiele wysiłku, dzięki czemu powstała naprawdę wspaniała praca naukowa, która praktykom daje gotowy schemat rozpoznawania i leczenia tych trudnych z punktu klinicznego chorób.
Background. Our previous studies have shown that short-term treatment with phenobarbital (PB) resulted in cytosine methylation of CpG sites on the p53 gene promoter in male Wistar rats’ liver. Furthermore, PB induced DNA-methyltransferases (DNMTs) activity was also demonstrated; being the enzymes that catalyze methyl group transfer to cytosine in CpG dinucleotides. Objective. Since DNA methylation is involved in regulating gene transcription and that DNMT1 is implicated in regulating DNA methylation, this study assessed whether PB-induced hypermethylation of the p53 promoter region was associated with an altered expression of p53 and Dnmt1 genes. Material and methods. Male Wistar rats received PB in three daily oral doses (at 24-h intervals) of 92,8 mg/kg b.w. x day-1. Levels of mRNA for p53 and Dnmt1 and levels of relevant proteins were respectively examined by Real-Time PCR and Western blot analysis. Results. Gene expression analysis revealed that exposure of Wistar rats to PB caused statistically significant alternations in the expression of tested genes. We found that both mRNA and protein expression of p53 was down-regulated, whereas expression of Dnmt1 (both mRNA and protein) was up-regulated after PB treatment. Conclusions. Suppression of p53 mRNA and protein expression, which is probably a result of epigenetic changes, (in particular aberrant p53 promoter hypermethylation), can be associated with tumour promoting activity of phenobarbital.
Among large husbandry animals, swine are the most predisposed to zearalenone (ZEA) intoxication, mainly because cereal is an important component of their diet. Studies performed so far (in vivo, in vitro) suggest that ZEA and its metabolites, which may appear due to ZEA biotransformation (especially α-zearalenole; α-ZOL), can modify signaling cascades of endogenous sex steroids, through either receptor or non-receptor mechanisms. Of all age groups of swine, immature gilts are particularly predisposed to zearalenone intoxication, as manifested by the occurrence of genital tract tissue dysfunction on exposure to ZEA. The intensity of the adverse effects observed at either systemic or local level in gilts, when compared to sexually mature swine females, suggest that specific age-dependent physiological conditions may exist, which determine the high sensitivity of gilts to exogenous estrogen-like compounds, including ZEA.
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