To define the development of herpes virus infection and morphological changes in the brain a upon a cerebrovascular accident. Methods. The experiments were performed on white mice weighing 18-20g. The animals were infected with type I HSV. Stroke was simulated after recovery and the rate of virus reactivation was determined. The rate of HSV production was evaluated by determination of viral antigens in Vero cell culture, PCR and dot-ELISA methods. The neurodegenerative process was confirmed by histological examination. Results. Reactivation of HSV-I was detected after the stroke. Histological study confirmed anincreased degree of neurodystrophic process around the hemorrhage, including hippocampus. A diagnostic value of the molecular methods has been proven in the detection of herpes infection in the biological samples (plasma, homogenates of animal organs). Conclusions. This study provided new data on the pathogenesis of herpes virus infection after acute stroke and its place in the development of complications. We have shown that the ischemic brain damage was a factor of type I HSV reactivation and it was characterized by a higher rate of neurodegenerative changes in hippocampus as compared to the isolated development of neuroinfection or impairment of cerebral circulation.

Background: Herpes simplex virus (HSV) is prevalent in today’s world population, and there is evidence of potential HSV reactivation in patients with immune deficiency induced by acute stroke. However, the data on the use of antivirals in the setting of stroke are scarce. The aim of this study was to evaluate the reactivation of HSV-1 in patients with stroke, using several methods, and to assess the efficacy of acyclovir in the treatment of experimental stroke. In the employed methodology, PCR and dot-ELISA were used to detect the occurrence of HSV-1 in patients with acute stroke. White mice were infected with HSV-1 and experimental stroke was simulated. The infected mice with stroke were subdivided into two groups: one of them received no treatment, while the other one was treated with acyclovir. The level of HSV-1 reactivation was determined by the methods used in human patients. The brain tissue of experimental animals was also subjected to morphological and morphometrical study. The results of such work reveal that, by the applied serological method, HSV-1 was found in all patients with stroke. Herein, the increased level of HSV-1 was seen in the brain tissue and blood in 100% of the experimental infected animals. However, the use of acyclovir suppressed reproduction of HSV-1. Hence, it can be concluded that clinical and laboratory studies have demonstrated the different sensitivity of Dot-Elisa and PCR, with the former being more sensitive. Moreover, the use of acyclovir in the experiment inhibited viral reproduction and further development of viral infection. Still, chemic lesions in the brain persisted.

Lead as any heavy metals may be found in soil, water, air, and is used in everyday life. Once in the body, it causes toxic effect, making the liver, which is one of the main organs of detoxification, suffer. Recently, the study of the action of not only ionic forms of lead, but also its nanoparticles, has become topical. The study aims at determining changes in the liver of rats and biochemical changes in their blood both at late term of exposure to nanoparticles of lead compounds and in the post-exposure period. The study was performed on 120 male rats of Wistar line, which were divided into two series, each series containing four groups. The first and the second groups of animals were intraperitoneally injected with colloidal solution of nanoparticles of lead sulfide of 10 and 30 nm in size, and the third group were intraperitoneally injected with a solution of lead nitrate. The fourth group of animals served as control. In the first series, the investigated substances were administered 60 times within 12 weeks. In the second series, after 60-fold administration of the investigated substances, the exposure was discontibued and animals were observed for 6 weeks-overall duration of 18 weeks. Histological, morphometrical and biochemical methods were used. The body weight was reduced in the rats exposed to PbS at week 12 of experiment and in rats exposed to both PbS and Pb(NO ) in the second series. Absolute liver weight increased at week 12 of experiment in all experimental groups. In the second series this value almost reached that of the control level. Relative liver weight in the animals of all experimental groups was higher than that in the control at week 12 of experiment. In the second series this value remained higher in rats exposed to PbS . After 12 weeks of exposure dystrophic changes in the liver were found in all experimental groups. At week 6 after the exposure (the second series) destructive changes in the liver decreased. Total protein, albumin, glucose, total lipids, cholesterol, triglycerides content in blood serum corresponded with morphological data. The experiment has demonstrated that the 12 weeks long exposure to lead nanoparticles had harmful effect on the liver. Within the postexposure 6-weeks period structural changes in the liver and biochemical changes in blood serum decreased. Biochemical changes in blood serum corresponded to the morphological data. By many parameters PbS had more pronounced harmful effect. Toxicity of PbS and Pb(NO ) were comparable.

Morphological data show that unithiolum and thiotriazolinum action decreases toxic effects of mercury chloride and are similar. They demonstrate pronounced activation of synthetic processes in sensory neurons and satellite cells of spinal ganglia. Mildronate also restores cell ultrastructure and has more pronounced effect on their energetic processes and interaction between neurons and satellite cells.

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Cadmium compounds are highly toxic substances characterized by mutagenic, genotoxic and carcinogenic effects, and having high cumulative properties. Application of cadmium nanoparticles (NPs) in medicine stimulates the study of their mechanism of action at the cellular level and at the level of organs and systems, determination of biomarkers of their action, particularly in comparison with the ionic form. The aim of the study was to compare the features of cytotoxic and genotoxic effects of cadmium sulfide (CdS) NPs of different sizes on cell cultures of different histogenesis with those of cadmium chloride (CdCl2). Materials and Methods: In this work, we used cadmium compounds in the nanoform: NPs CdS of 4–6 nm and of 9–11 nm in size; and in the ionic form: CdCl2. The studies were conducted in vitro in cell lines — IMR-32, НEК-293 and MАEC. To count viable cells we compared the results of three basic tests: MTT (methyl tetrasolium test), SRB (sulforhodamine B test) and NRU (neutral red uptake test). We evaluated the genotoxic effect of the substances studied in vitro using DNA comet assay in alkaline conditions. Results: CdS NPs and CdCl2 demonstrated pronounced dose-dependent cytotoxic effect in MАEC, НEК-293 and IMR-32 cell lines, by impairing membrane permeability, functioning of mitochondria and lysosomes, and inhibiting the function of protein synthesis. Cytotoxic effect of CdCl2 was the most pronounced, this effect of CdS NPs of 9–11 nm in size being the least pronounced. The comet DNA assay in alkaline conditions revealed a statistically significant increase in DNA comet index when exposed to CdCl2 and CdS NPs in comparison with the negative control, which indicates their genotoxic effect. CdS NPs of 4–6 nm in size showed a more pronounced effect in comparison with those of 9–11 nm in size. Conclusion: Elucidation of mechanisms underlying the implementation of toxic effects of cadmium NPs will help in assessing the potential risks associated with their use in industry and developing effective preventive measures. For instance, when planning in vivo studies for toxicological evaluation of nanomaterials and nano-substances containing NPs of cadmium, it is necessary to investigate the mutagenic and carcinogenic risks and to take into account the high likelihood of neurotoxic and cardiovasotoxic effects, along with nephrotoxic effects, since high cytotoxic activity of the investigated compounds of cadmium was detected on the cells of the MАEC line (endothelial origin) and IMR-32 (neuronal origin).

The article is devoted to the characteristics of the myocardium restructuring under the influence of 0.01 LD50 mercury (II) chloride, in rats, under subchronic exposure, and the correction of the detected changes. In the work, the structural and metabolic reorganization of myocardium was studied by way of general histological, histochemical and electron microscopic techniques. Herein, administration of Unithiolum reduces the severity of reactions to toxic effects of mercury salts: decreases the intensity of inflammation in the myocardium, improves microcirculation, connective tissue and mitochondrial membranes status and reduces cardiomyocytes apoptosis. Quercetinum has a normalizing effect on the myocardium structure, reduces energy imbalance in the myocardium, and stabilizes mitochondrial membranes. Both Unithiolum and Quercetinum promote intracellular ultrastructures recovery in cardiac myocytes and in endothelial cells, and enhance the regeneration of myofibrils.

Introduction: There is an increasing number of cases of congenital hypothyroidism. One of the most common complications of hypothyroidism is damage to the cardiovascular system, which in 30-50% of patients leads to the development of arterial hypertension. The aim: studying the features of the ultrastructure of myocardial capillaries in mature rats with hypothyroidism. Materials and methods: Experiments were conducted on 40Wistar line rats with congenital hypothyroidism: juvenile young (45-day) and sexually mature (100-day) rats, as well as intact animals of the corresponding age. While extracted from the experiment rats of all experimental groups had their arterial pressure measured using a plethysmograph while the development of hypothyroidism was controlled by the immune-enzymatic method. Electron microscopic examination of the left ventricular myocardium and morphometric study of volumetric and quantitative densities, cross-section area, and form factor of micropinocytotic vesicles were conducted. Results: In the sexually mature rats with congenital hypothyroidism the quantitative density of the capillaries in the myocardium decreases. Activation of transcytosis is accompanied by significant violations of vesiculation. Some of the endothelial cells of experimental animals contain a moderate amount of transport vesicles, while others are overfilled with these structures and desquamate into the lumen. In older rats with congenital hypothyroidism there is a further dilution of capillaries, the development of hypoxic state in them, mucinous edema of interstitial space, decrease of biosynthetic and transport processes activity. Conclusions: In young (45-day) rats with congenital hypothyroidism the direction and expressiveness of compensatory processes is to enhance the transcytosis processes. Dystrophicdestructive changes are manifested by apoptosis in some endothelial cells, decrease in the number of biosynthetic organelles, lysis and edema of their cytoplasm. In sexually mature (100-day) rats with congenital hypothyroidism destructively-dystrophic processes in the blood capillaries of the myocardium are approximately balanced with compensatory-adaptive.