[Evaluation of the effect of mazindol on the metabolism and lipolysis in obese women].
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Biomedical subjects
Publications and source records attributed to D Piskorska.
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A series of nine glycosylamines and an Amadori compound and their N-nitroso derivatives were synthesized. The structures were ascertained by spectroscopy and elemental analysis. The N-nitroso compounds were further characterized by denitrosation with hydrogen bromide-acetic acid, followed by detection of the liberated NO by a chemiluminescence detector. N-Nitroso derivatives of N-p-nitrophenyl/p-methylphenyl/p-carboxyphenyl pentosylamines, N-p-methylphenyl-1-deoxy-D-fructosylamine (Amadori compound) and N-3-ethylindole-D-xylosylamine were shown to be directly-acting mutagens in Salmonella typhimurium TA100. The activity of some of the compounds was similar to that of N-ethyl-N-nitrosourea. Their mutagenic activity was shown to be dependent on the structure of the amine and the sugar moieties and requires the presence of free hydroxyl groups in the sugar. The mutagenicity of N-nitrosoglycosylamines was attributed to their hydrolysis to arene diazonium cations. Their formation was detected via azo-coupling with N-ethyl-1-naphthylamine, using spectrophotometric and mass-spectrometric analyses. Our data implicate arene (alkyl) diazonium cations as the ultimate mutagens of N-nitrosoglycosylamines and N-nitroso Amadori compounds, a little explored class of N-nitroso compounds which may be formed in vivo.
Adrenergic modulation of lipolysis was determined in obese and lean women. Epinephrine was infused alone, or in combination with propranolol, or with phentolamine. In both obese and lean subjects slight alpha- and prevalent beta-adrenergic lipolytic responsiveness was observed. alpha-adrenergic blockade by yohimbine potentiated lipolysis and exercise energy expenditure. Yohimbine application during the slimming treatment increased weight loss without side effects.
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The effects of low doses of lead and cadmium on the activities of glyoxalase I and glyoxalase II in liver and brain of male Wistar rats were examined. Generations P, F1 and F2 received lead acetate and cadmium acetate in drinking water. The doses were as follows: group I-Pb 5 ppm, group II-Pb 50 ppm, group III-Cd 0,1 ppm, group IV-Cd 5 ppm. group V-Pb 5 ppm + Cd 0,1 ppm, group VI-Pb 50 ppm--Cd 5 ppm. The control group received sodium acetate with water. P population received Pb and Cd for 40 days before fertilization, and then the pregnant females were given the same doses until the end of pregnancy. Animals of F1 and F2 generation were killed after 30, 60 or 90 days. In liver and brain homogenates the activities of glyoxalase enzyme system were determined by the spectrophotometric method at 240 nm. A little inhibition of glyoxalase I was observed in rats that were given lead for 30 days, while in rats treated for 60 and 90 days the activities of glyoxalase I increased. Glyoxalase II was activated both by lead and cadmium in all groups. In vitro examinations demonstrated that lead and cadmium inhibited the activity of glyoxalase I and activated glyoxalase II.
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Determinations were made of glyoxalase I and glyoxalase II acitivity in the liver of mice (BDF1 and DBA2 strains) bearing sarcoma 180 and L1210 leukemia in ascites form. A progressive decrease in the both glyoxalase I and glyoxalase II activities to about 40--60% of that of the control groups was observed within the developing period 8--9 days. Test results are interpreted in the light of the postulated role of this enzyme system in cell division and in the tumor development process.
Glyoxalase I bound to Sepharose 4B was used for synthesis of S-lactoyl-glutathione. The bound enzyme does not lose its activity during several months storing and can be used many times for synthesis of S-lactoyl-glutathione. This reaction product can be used as a substrate for glyoxalase II without any further purification.
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BACKGROUND: Water immersion stress (WIS) in rats causes decrease in deformability of red blood cells (RBC). We hypothesize that this phenomenon is mediated by reactive oxygen species. Since tirilazad mesylate (U74006F) is a potent scavenger of free oxygen radicals, the aim of this study was to investigate possible influence of this drug on WIS induced decrease in RBC deformability in rats. MATERIAL AND METHODS: The rats were injected i.p. with tirilazad mesylate in a dose of 10 mg per kg body weight or vehiculum at the beginning of the experiment and immersed in water at 23 degrees C to the depth of xyphoid for 5 h. Control rats were kept in normal environment. After 6 h blood samples were collected for examination. An elongation index of RBC measured by Rheodyn SSD (Myrenne GmbH, Germany) was used as a parameter of deformability. Lipid peroxidation products have been assayed in RBC by BIOXYTECH LPO-586 kit. RESULTS: Tirilazad mesylate prevents a decrease in RBC deformability, but does not prevent an increase in concentration of lipid peroxidation products in erythrocytes during WIS. CONCLUSION: Positive effect of tirilazad on stress induced decrease in RBC deformability is not related to inhibition of lipid peroxidation within the erythrocytes.
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