Catabolism of purine mononucleotides to hypoxanthine and xanthine in the liver is enhanced in rats resuscitated after a 6.5-min asphyxia. Reduced incorporation of 14C-hypoxanthine into these nucleotides 30 min, 1, and 3 days after resuscitation attests to its disturbed reutilization. This probably promotes activation of the xanthine oxidase reaction, leading to purine deficit and hyperproduction of reactive oxygen species. Key Words: hypoxanthine; postresuscitation disturbancesAccumulation of hypoxanthine (HX) in tissues during the postresuscitation period results from enhanced catabolism of purine mononucleotides [3,4]. Activation of xanthine oxidase reaction renders this process irreversible [9]. Moreover, it has been previously hypothesized that in vivo activation of xanthine oxidase reaction leads to hyperproduction of reactive oxygen species [3,4,6]. An alternative pathway is reutilization of HX. Apart from hepatogenic HX, the liver metabolizes HX delivered by the blood [141, therefore disturbances in HX metabolism can have grave consequence for the whole organism. In the present study we evaluated the efficiency of HX reutilization in the liver of resuscitated rats. MATERIALS AND METHODSExperiments were carried out on 140 male rats weighing about 200 g. They were resuscitated after 6.5-min asphyxia as described previously [8]. They were narcotized with ether 30 and 90 min, 6 and 24 h, and 3, 7, and 21 days after resuscitation, a and the liver was ex vivo fixed in liquid nitrogen. Control rats were subjected to the same procedures except for asphyxia and resuscitation. 14C-HX was injected intravenously in a dose of 740 kBq/kg body weight 25Central Research Laboratory, State Medical Academy, Omsk min prior to f~ation. The liver was processed as described elsewhere [51.It is known that HX is converted not into inosine, but into inosine monophosphate and then into other nucleoside-monophosphates (NMP): adenylosuccinate, adenosine monophosphate, xanthosine monophosphate, guanosine monophosphate [9]. NMP are then phosphorylated to nucleoside di-and triphosphates (NDTP). Hence, reutilization 14C-HX can be assessed only by measuring radioactivity not only of major mononucleotides (ATP and GTP) but also of all purine mononucleotides; NDTP and NMP should be measured as two independent pools. The content of HX and xanthine in the liver was measured as described elsewhere [13], and label incorporation into purine NMP and NDTP and their content were determined by our methods. The data were processed statistically using the Student and Wilcoxon--Mann--Whitney tests and Spearman correlation coefficient [2]. RESULTSCatabolism of NMP and NDTP in the liver of resuscitated rats is enhanced, as evidenced by reduced content of these nucleotides and accmnulation of HX and xanthine (Table 1). Hypoxanthine is a common catabolite of all purine mononucleotides [11,12]. It can be hypothesized that HX formed during asphyxia

No abstract

The research objective was to evaluate the morphofunctional state of the adrenal glands in laboratory animals in conditions of acute and chronic intoxication with cypermethrin. Studies were performed on 140 male rats of the Wistar line. To simulate an acute intoxication cypermethrin was single injected into the stomach in a dose of half of LD50 followed by observation of the animals for 30 days. In the study of chronic intoxication cypermethrin was administered to rats in a dose of 1/100 of LD50. The experiment has lasted for 120 days.At the initial stage of the experiment the acute intoxication of rats with cypermethrin caused hyper- and then hyposecretion of adrenocorticotropic hormone. The content of progesterone in the blood serum and adrenal tissue decreased in animals. During the first three days after the poisoning there was an increase in the concentration of corticosterone in the blood serum. To the end of the 7th day the concentration of this hormone in adrenal tissue decreased sharply and did not reach the control background after a month. Chronic intoxication with cypermethrin caused hypersecretion of adrenocorticotropic hormone for two months with the subsequent normalization of its level in the blood. The disturbance of progesterone synthesis in the adrenal glands during chronic intoxication is indicated by fluctuation of its concentration in blood 30 days after the start of the experiment. There was found high level of corticosterone in blood and adrenal glands for two months, and then it decreased to a control level. Morphological criteria for amplification and then suppression of adrenal function are the dimension of endocrine cells and their nuclei, the intensity of cell vacuolation suggesting the degree of lipids accumulation, and the severity of blood filling in the vessels of the beam and reticular zones.

A b s t r a c tThe world market of synthetic pyrethroids is estimated more than at 2.5 bn. dollars and will grow in the next years. Numerous works of domestic and foreign authors are devoted to toxicology of pyrethroids, however the issues related to pathogenesis of an acute poisoning of animals with pesticides of that group as well as the principles of laboratory diagnostics at an early stage of intoxication and pathogenetic therapy at poisoning warrant further investigations. For many years deltamethrin has been successfully used in plant growing as well as in animal husbandry creating a poisoning hazard in case of violation of treatment regulations. Morbidity and clinical outcome depend largely on severity of functional endocrine and immune systems disorders. The purpose of the study was to determine dynamics of adaptive and compensatory reactions in animals at an early stage of an acute intoxication with deltamethrin. In experiment white laboratory rats as an established mammal model in biomedical research were used. The experiment was performed on male rats (weight of 180-200 gr) arranged in 6 groups (of 10-12 rats each). Animals from groups II, IV and VI have been subjected to an acute peroral intoxication with deltamethrin (Butox 50, Intervet, Netherlands) in a dose of 43.5 mg/kg of body weight. Rats of groups I, III and V served as control. Rats from different groups were put out of the experiment sequentially: I and II -in a day; III and IV -in three days; V and VIin a week after the beginning of the experiment. Glucose content was estimated in whole blood of rats, and concentration of insulin and corticosterone was assayed in blood serum. Pieces of animal timus were fixed in 4 % neutral formaldehyde, dehydrated in alcohols with the increasing concentration and embedded into paraffin. Histologic sections at 3-5 microns in thickness were made with the rotational microtome and stained with haematoxylin and eosin, and also according to Van-Giezon. For identification of mast cells the histologic sections were stained with Bismarck brown to Shubich. Increase in blood corticosterone, insulin and glucose levels by 46.3 (p = 0.0001), 31.9 (p = 0.0139) and 25.6 % (p = 0.0052), respectively, was found in a day after poisoning with deltamethrin. On day 3 after poisoning the blood concentration of corticosterone and glucose in rats remained high along with a decrease in insulin content. Hypocorticosteronemia and hypoglycemia were observed on day 7 after poisoning, with the insulin level close to control values. Corticosterone and glucose content has been reduced by 17.3 (p = 0.0407) and 19.8 % (p = 0.0267), respectively, compared to control. Photomicrographs showed a reduction in the number of thymocytes, activation of apoptosis, an increase in quantity of mastocytes along with an intensification of degranulation as well as development of haemodynamic disorders in thymus when poisoning rats. In a week after intoxication the thymocytes level was partially restored. No animal died during experiment which evidences th...