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The effect of different types of dietary fat on muscular acetylcholinesterase (Ache) activity was studied in rats. Enzyme activity was determined in two leg muscles: red soleus and white gastrocnemius. After one week of feeding fat-free diet (20% of energy from protein with casein as its source and 80% of starch as carbohydrate) rats were fed one of four isocaloric diets (16 kJ/g; 20% protein, 60% carbohydrate and 20% fat) differing in source of dietary fat (sunflower oil - S group; lard - L; palm oil - P; rapeseed oil - R). There were no significant differences in Ache activity in soleus and gastrocnemius after fat-free regimen. Diet intake containing fat during the first week evoked decrease in Ache activity in group L in soleus and in groups S, L and R in gastrocnemius. Palm oil diet feeding did not change Ache activity as compared to that observed after fat-free diet. After subsequent two weeks of supplying diets containing fats Ache activity increased in soleus in all dietary groups; in gastrocnemius it increased in groups S and L. Thus, after three weeks of consuming fats from different sources in both muscles significant differences in Ache activity among various dietary groups were not observed; its activity in soleus did not differ significantly from that observed after fat-free diet in all groups, in gastrocnemius it remained significantly lower only in R group. These results suggest that the influence of dietary fat on muscular Ache activity could be a transient phenomenon and depends on muscle type. However, taken into consideration different dependence of Ache muscular isoforms on factors regulating, adaptations based on changes in their relative participation in overall Ache activity could not be excluded.
The activity of AChE in plasma, the brain and spinal cord and of NTE in the brain and spinal cord was determined after 1, 7, 14, 21 and 28 days in 30 hens (Leghorn) intoxicated once with DFP at a dose of 1 mg/kg b.w. The activity of AChE decreased during 24 h after intoxication in plasma to 12%, in the brain to 24% and in the spinal cord to 32%. Then the activity of this enzyme increased and after 28 days after intoxication was 107% in plasma, 84% in the brain and 91% in the spinal cord. The activity of NTE decreased after 24 h to 9% in the brain and to 18% in the spinal cord and then increased to attain 73% in the brain and 61% in the spinal cord after 28 days.
The aim of the study was to investigate acetylcholinesterase-immunoreactive neurons in the CA1 area of the hippocampus and in the striatum (CS) of rats receiving rebaudioside A (RebA) for 15 days. RebA is a steviol glycoside used in the production of sweeteners, and it has been shown that glycosides affect memory and learning processes. RebA was administrated to adult rats for 15 days at 1 mg of glycoside/ml of water (group I) and 2 mg of glycoside/ml of water (group II). An indirect immunohistochemical peroxidase-antiperoxidase reaction was performed on frontal slides containing the hippocampus and CS with the use of a monoclonal antibody against AChE. Neurons immunoreactive for the protein were assessed morphologically and morphometrically in hippocampal area CA1 and in the CS. Microscopical observations did not reveal significant morphological changes in immunopositive neurons, which suggests that the glycoside had no neurotoxic effect of these cells. Morphometric analyses did not show changes in the density of AChE-immunoreactive neurons. On the other hand, a decrease in reaction intensity was demonstrated in hippocampal area CA1 in group I and in the CS in both groups of animals receiving RebA. The results of our preliminary studies suggest that RebA affects cholinergic neurons.
Oznaczano aktywność esterazy acetylocholinowej (AChE) we krwi i w mózgu szczurów narażonych na ołów, fenitrotion i foschlor oraz ołów z fenitrotionem i ołów z foschlorem. Wykazano zróżnicowany wpływ octanu ołowiu(II) podanego jednorazowo w dawce 250 mg/kg m.c. i w sposób frakcjonowany (przez 5 dni po 50 mg/kg m.c.) na aktywność cholinoesteraz. W intoksykacjach mieszanych ołów nasilał i przedłużał proces hamowania AChE wywołany przez fenitrotion oraz przedłużał reaktywację tego enzymu. Natomiast po podaniu ołowiu z foschlorem między 6. godziną a 21. dniem doświadczenia występowały nieregularne zmiany o różnym nasileniu w aktywności AChE we krwi i w mózgu. Bardziej nasilony spadek aktyw­ności tego enzymu był w grupie szczurów narażonych na octan ołowiu(II) w dawce frakcjono­wanej i foschlor niż w grupie zwierząt intoksykowanych jednorazową dawką octanu ołowiu(II) i foschloru.
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