Search

The aim of this paper is to investigate the influence of Thiocetam on morphological changes in the liver of rats and on biochemical changes in their blood after exposure to lead nanoparticles and compounds. The liver is an organ that performs a number of functions, such as the synthesis of enzymes, hormones, plasma components and the neutralization of toxins. It is involved in many metabolic processes in the body. In undertaking this, colloidal solutions of lead sulphide nanoparticles at dosages 10 nm and 30 nm were injected into two groups of rats, PbSnano1 and PbSnano2, respectively, while group Pb(NO3) received subcutaneously a solution of lead nitrate in ion form in a dose of 1.5 mg/kg (0.94 mg/kg lead, in lead equivalent). After 60 administrations (12 weeks) of the studied substances, the exposure was discontinued and the animals were observed for 18 weeks. Subsequently, half of each group received Thiocetam by injection (for 6 weeks at a dose of 250 mg/kg) while the other half did not. We then assessed the mean body weight, absolute and relative liver weight, blood biochemistry values (total protein, albumin, glucose, total lipids, cholesterol, triglycerides levels in blood serum) and morphological changes in hepatocytes (morphological slides, nuclei cross-sectional area and cytoplasm cross-sectional area). The outcome of this work showed that the mean body weight of animals exposed to nanoparticles with Tiocetam did not differ from that of animals exposed to nanoparticles without pharmacological correction, but relative liver weight was statistically significantly higher than the corresponding values in rats without pharmacological correction. The morphological picture in all study group animals was characterized by the normalization of microvessel blood filling, structure of hepatic plates, disappearance of infiltration with lymphocytes and histiocytes. No dystrophic changes in hepatocytes were found. All this indicates the feasibility of preventive measures during exposure to lead nanoparticles, by administering Thiocetam. In both series of animals exposed to lead nanoparticles (PbSnano1 and PbSnano2), the cross-sectional area of the hepatocytes cytoplasm and the cross-sectional area of the hepatocytes nuclei were smaller than just after exposure, but in the series with Thiocetam adminstration, all the values did not differ from those in the control.

Increasing interest in nanomaterials can be explained by their broad involvement in many fields of industry and medicine. It is known that carbon black and crysotile asbestos behave like nanosized objects. They are wide spread in environment and have close contact with living organisms. The aim of our study was to define the effects of carbon black and crysotile asbestos on structures of the developing organism. We used chicken embryos as a model for our study. Total amount of 77 eggs was divided in three groups: one control and two experimental with introduced carbon black and asbestos respectively. Researched materials were injected in the yolk on the third day of incubation and tissues for study were taken during early, middle and late stages of incubation. Histological and electron microscopy methods were used. Carbon black and asbestos introduction caused underdevelopment of embryos and vessels depletion in blood islands of the yolk sac. Asbestos slowed down angiogenesis. Soot particles caused integrity violation of vessels and led to extravasation. The manifestations of soot influence were damages to blood circulatory system and structural disorders on cellular level. Introduction of chrysotile asbestos mostly resulted in compensatoryadaptive reactions like increasing in hematopoiesis and transcytosis in endotheliocytes.

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.

The study of herpetic infection is a topical problem. Although the peculiarities and consequences of acute HSV-I infection in the brain are quite well-studied, little is known about the damage to other organs which are not a source of latent HSV-I infection, the liver in particular. The current study is aimed at determining the ultrastructural changes in murine liver following HSV infection and stroke. Liver samples obtained from four groups of animals were studied: 1) intact mice; 2) mice with stroke; 3) mice infected with HSV-I; 4) mice aflicted with HSV-I and subsequently simulated stroke. The study showed the reproduction of the virus in hepatic endotheliocytes, although no virions were detected in the hepatocytes. Therefore, the described changes were considered the consequences of the infectious process. Pathological changes of hepatocytes consisted of deformation and fragmentation of the nuclei, as well as accumulation of osmiophilic granules, lysosomes and lamellary bodies. Latent HSV-I infection may reactivate in liver after the stroke, potentially causing the complications of the underlying disease.

We examined toxic action of 10.9 μM mercury(II) chloride on cultured IMR-32 neuroblastoma cells and possible protective effects of a cardioprotector, mildronate (tested concentrations 0.01 to 10.0 mg/ml of culture medium) under such experimental conditions. Isolated addition of mildronate to the medium did not induce considerable negative effects (number of dead cells did not exceed 8-10% of their total number at all concentrations used). In the case of isolated action of HgCl2, about half of cultured IMR- 32 cells died (on average, 55.8 ± 1.6% of the cells remained viable). Mildronate in a 0.01 mg/ml concentration did not manifest a significant protective action, but at doses 1.0 and 10.0 mg/ml the mean number of living cells in the presence of HgCl2 reached nearly 80%. Thus, mildronate demonstrated relative safety in vitro and a significant protective effect under conditions of intoxication by low doses of mercury.