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EN
Deformability and activity of the enzymes: acetylcholinesterase (AChE) and dehydrogenase glucose-6-phosphate (G-6-PD), were assayed for RBC enriched in immature reticulocytes. Reticulocytosis was evoked by administration of two different drugs: recombinant human erythropoietin (rHuEPO) and phenylhydrazine (PHZ) to two groups of Wistar rats. After treatment with the former compound, a group of animals exhibited 17,33 % reticulocytes in blood whereas a group of rats treated with the latter drug reached 57,66 % of these cells in blood. A marked decrease in RBC deformability was found in both groups of animals. AChE did not significantly change activity neither in PHZ-treated nor in rHuEPO-treated rats, whereas G-6-PD activity was significantly decreased in the PHZ-treated group.
EN
Eighteen maleWistar rats were divided into 3 groups of 6 animals each. Two groups received different intraperitoneal doses of TCDD (0.75 and 8Fg) in DMSO solution and the third group (control) received only DMSO on days 0, 7 and 14. On day 21 the animals were sacrificed, and then blood tests, pathological examination and CYP1A1 activity measurement were performed. In rats that received a high dose of dioxin (8 Fg) hepatic lobules revealed parenchymal degeneration and vacuolization of hepatocytes was observed, and also an increased CYP reaction was found in central parts of lobules, around the central vein. The reaction in control and low dose groups was weak. The resorufin level was significantly (P<0.05) higher in the group receiving a low dose of dioxin as compared to the control group. The study confirmed that TCDD damages the rat liver in a dose-dependent manner. Administration of high TCDD doses causing major liver damage also damaged CYP1A1 (based on higher resorufin levels in epiluminescence). TCDD activates CYP1A1, which was confirmed by increased immunohistochemical reactivity of central areas of hepatic lobules.
EN
We followed changes occurring within bone tissue and marrow cells during the process of colchicine-induced ectopic bone development and its resorption inside the marrow cavity of the rat tibia. To stimulate ectopic bone formation male Wistar rats were i.p injected with 0.5 or 1mg/kg b.w. of colchicine orwith a 100 Fg intra-bone injection.Not all subjects responded to colchicine with ectopic bone formation in the marrow cavity, even among individuals belonging to the same strain. The kind of response in a given animal depended on the dose and site of colchicine administration. During 10 days of the experiment an increase in the occurrence of micronuclei in the polychromatic erythrocytes residing in the bone marrow (even 40-fold) was observed, indicating high genotoxicity of colchicine (at a dose of 1 mg/kg b.w. i.p. or 100 Fg intra-bone injection). An increase in the frequency of emperipolesis in megakaryocytes between the 4th and 8th days of the experiment was caused by the toxic action of colchicine and may indicate the labilisation of cell membranes and microtubule depolymerisation.
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