Can the function of the extirpated amygdaloid complex be compensated for by the transplantation of embryonic nerve tissue?

In 20 white rats bilateral coagulation of the amygdalar complex was produced; on the fifth day to one half of them transplantation was performed by introducing stereotaxically on the left side 0.2-0.5 mm3 of the brain embryonal tissue from the corresponding area of the amygdala of 20-days embryo; in control saline was administered. After two months the rats were sacrificed to determine the activity of antiradical defense by superoxide dismutase (SOD) and the level of lipids peroxide oxidation (LPO) in the cerebral cortex. The transplantation decreased LPO even more and increased SOD as compared to amygdalectomy, e. i. caused still greater deviations from the norm (in this meaning--paradoxal effect), what apparently corresponds to intensification of adaptative-compensatory processes caused by amygdalectomy. The transplantation did not reverse the rats behaviour to the initial one and did not eliminate memory defect in the test of conditioned reaction of passive avoidance (like pyrazetam); it had different direction influence on "drinking under current" in conflict situation, only in particular cases approaching it to the norm.     

The mechanism of superoxide dismutase functioning: a multicenter model

A new model of superoxide dismutase (SOD) functioning has been proposed on the basis of recent data. This model takes into account both experimental data and results of quantum mechanics calculations. One substrate molecule (superoxide radical) binds copper ion in active center of SOD, and the second superoxide radical interacts with a peripheral region of the enzyme. Uncoupled electron from the active center is transferred to the peripheral superoxide anion. This results in formation of oxygen molecule in the active center, and of hydrogen peroxide molecule in the peripheral region.     

Lectin histochemistry for detecting cadmium-induced changes in the glycosylation pattern of rat placenta

Cadmium (Cd) is an industrial and environmental pollutant that produces toxic effects on gametogenesis, pre- and post-implantation embryos, and the placenta. Because the effects of acute Cd intoxication on the placenta are not well understood, we investigated changes in its glycosylated components in Cd treated dams at days 4, 7, 10 and 15 of gestation using lectin histochemistry. CdCl₂ was administered to pregnant rats; control animals received sterile normal saline. Placentas were processed for DBA, Con A, SBA, PNA, UEA-I, RCA-I and WGA lectin histochemistry to evaluate changes in the carbohydrate pattern of the placenta that might modify cell interactions and contribute to embryonic alterations. Lectin binding was analyzed in the yolk sac; trophoblast giant cells; trophoblast I, II and III; spongiotrophoblast cells and endovascular trophoblast cells in the chorioallantoic placenta. Our lectin binding patterns showed that Cd caused alteration of SBA and DBA labeling of trophoblast-derived cells, which suggested increased expressions of α and β GalNAc. Cd also caused decreased UEA-1 binding affinity, which indicated fewer α-L-Fuc residues in placentas of Cd treated dams. The nonreactivity in trophoblast I of the control placentas incubated with Con-A contrasted with the labeling in placentas of experimental dams, which indicated increased expression of terminal α-D-Man, and α-D-Glc residues. We found that Cd altered the reactivity of placenta to several lectins, which indicated modification of the glycotype presented by the fetal component of the placenta. We report that Cd exerts a deleterious effect on the glycosylation pattern of the placenta.     

The individual differences in responses of cancer patient blood cells on radiation treatment during the chemotherapy

A comparative comet-assay study of X-ray influence on DNA of leukocytes of peripheral blood from both cancer patients in the course of chemotherapy and on healthy donors was carried out. The amount of DNA registered in comet tails of blood samples from 18 healthy donors was between 0.8-3.6%. The mean value was 2.9 +/- 0.5%. In the preparations of cancer patients, an increase in comet tail DNA was observed for each chemotherapy course and in each subsequent course compared to the previous one. The individual variations were found in the level of DNA damage in the response to the administration of cyclophosphane, of methotrexate, of 5-fluorourocil (CMF protocol). The X-ray radiation (4 Gy) challenge test of blood cells showed an increase in comet tail DNA, the dynamics of radiation-induced lesions varying between individuals. The combined use of X-ray radiation and of the comet-assay in evaluating the capacity of the defence systems of the whole blood cells during chemotherapy let us to hold the monitoring of the state of genome of leukocytes without their isolation. This approach enables additional information on leukocyte genome to be rapidly obtained.     

Study of DNA-binding proteins in mitochondria of rat liver gamma-irradiation

Acid-soluble proteins were isolated from the liver mitochondria of control and irradiated (8 Gy) rats. By means of electrophoresis in 15% polyacrylamide gel, these proteins were separated into more than 20 polypeptides of molecular masses between 10 and 120 kDa. The irradiation of rats with a dose of 8 Gy led to changes in the polypeptide content of mitochondrial acid-soluble proteins in the postradiation period. It was found that the liver acid-soluble proteins of control and irradiated rats were able to form nucleoproteid complexes with DNA at the physiological NaCl concentration. It was shown that along with mitochondrial acid-soluble proteins, proteases were also released, their activity increased in the presence of DNA. Twenty four hours after irradiation of rats with 8 Gy, the activity of proteases cleaving mitochondrial acid-soluble proteins decreased. Probably, the acid-soluble proteins and DNA-activated proteases of mitochondria are involved in the regulation of the structural organization and functional activity of mitochondrial DNA.     

Analysis of the level of cyclic adenosine-3',5'-monophosphate in structures of the 'informational' and 'motivational' system of the rat brain during active conditioning

The content of cyclic adenosine-3',5'-monophosphate (cAMP) was studied in structures of the "motivational" and "infromational" systems of rat brain after the active avoidance conditioning procedure in rats. Three groups of animals were examined: naive rats, trained (conditioned) rats, and group of the active control presented with uncombined conditioned (light) and unconditioned (electric footshock) stimuli. The content of cAMP was determined in the frontal cortex, hippocampus, amygdala, and hypothalamus of both hemispheres immediately after the retrieval of conditioned reaction one day after conditioning. A significant increase in cAMP level was bilaterally observed in the hypothalamus in the group of active control, and in both hippocampi and the right frontal cortex in the conditioned animals. Positive correlations between the cAMP levels in symmetrical regions of the frontal cortex, amygdala, and hypothalamus were revealed in all the examined groups. Additionally, intra- and interhemispheric correlations were found in the active control and conditioned rats. Patterns of correlation were specific for each of these groups. The observed phenomenon is discussed in term of involvement of "informational" and "motivational" brain structures in the mechanisms of adaptive behavior.     

Effects of amyloid beta peptide (25-35) on the behavior of rats in a radial maze

Impairment of cognitive functions, particularly long-term (episodic) and working memory, is one of the earliest prognostic symptoms of Alzheimer's disease, both cognitive impairment and neurodegeneration being mediated by amyloid-beta neurotoxicity. Effects of intracerebroventricular administration of amyloid-beta peptide (25-35) [A beta(25-35)] to rats on the retention of previously learned task in an 8-armed radial maze was studied. A beta(25-35) was injected bilaterally, at doses of 15 or 30 nmol/rat, 7 days after the preliminary learning. The performance in the maze was tested 60 days after the surgery. A beta(25-35) impaired the short-term memory, with no significant effect on the long-term memory. No dose dependence could be demonstrated.     

Indices of lipid free-radical oxidation and of antiradical protection of the brain--the neurochemical correlates of the development of the general adaptation syndrome

The stage of rat long-term adaptation to chronic emotional-pain stress is characterized by an increase of superoxide dismutase brain activity and superoxide-scavenging blood serum activity, accumulation of fluorescent products of free-radical oxidation, reduction of phospholipids and cholesterin contents in the brain lipid extracts. In the process of prolonged adaptation to the continuing chronic emotional-pain stress three periods are singled out, each of which with a definite correlation of characteristics of vegetative functions, behaviour, intensity of free-radical oxidation and antiradical defence.     

Superoxide elimination activity and the transferrin-ceruloplasmin antioxidant system in the blood serum in chronic emotional-pain stress and the administration of dimethyl sulfoxide in rats

The influence of emotional painful stress (EPS) and dimethyl sulfoxide (DMSO) treatment on ceruloplasmin-transferrin (Cp-Tr) antioxidant system and superoxide dismutase-like activity (SODLA) of the rat serum was studied. No changes in Cp-Tr and SODLA were observed in EPS. On the contrary, DMSO treatment was followed by a decrease in Cp-Tr activity and an increase in SODLA. It is suggested that Cp-Tr and SODLA systems are two interacting antioxidant systems of the serum.