No 2 (2019)

In recent years, there has been an increase in the prevalence of neurodegenerative diseases including Parkinson’s disease (PD). It is characterized by progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to disability of patients and large financial costs of the treatment and rehabilitation. In this regard, the understanding of the environmental factors causing this disease, the development of adequate experimental models for studying its pathogenesis, and the search for strategies to prevent its development, as well as possible neuroprotective drugs, have fundamental scientific value. Although some researchers believe that genetic mutations and aging of the population are the main factors for the development of PD, a lot of studies have shown that PD may be caused by exposure to a number of toxins which enter the body from the environment. This review discusses the main toxic substances that cause the development of PD and, therefore, are used to model this disease in animals and cell cultures, as well as the mechanisms of action of neurotoxins, and the advantages and disadvantages of specific models.

The possibility of blood lipid metabolism recovery in rats after intoxication with carbon tetrachloride using Kalifen® extract from viburnum and the comparison preparation Legalon® has been shown. The experiments were conducted on male white rats of the Wistar line in standard vivarium conditions. Animals were divided into 5 groups: 1st group - control; 2nd group - introduction of carbon tetrachloride for 4 days; 3rd - introduction of carbon tetrachloride for 4 days followed by cancellation within 7 days; 4th group - introduction of carbon tetrachloride for 4 days followed by introduction of Kalifen® for 7 days; 5th - introduction of carbon tetrachloride for 4 days followed by introduction of Legalon® for 7 days.
It has been found that intoxication with carbon tetrachloride was accompanied by the development of severe hypercholesterolemia, as well as the increase in the content of the total fraction of lipoproteins of very low density with reducing the concentration of high density lipoproteins in the serum. There were a decrease in the main structural phospholipids and metabolically active fractions, an increase in the number of triacylglycerols, free fatty acids, and lysophospholipids.
During the cancellation of carbon tetrachloride within 7 days lipid metabolism indicators did not recover, indicating that free-radical reactions occur even in the absence of the toxicant. The introduction of Kalifen® and Legalon® in animals under the conditions of the withdrawal of the toxicant contributed to the recovery of the studied parameters to control values, but the most pronounced effect has been manifested using Kalifen®.

The article presents the results of the experimental toxicological study of rats poisoned with uranyl acetate dihydrate (300 mg / kg body weight). The aim of this study was to develop methodological approaches to the early detection of acute toxic kidney damage on the basis of the dynamics of some biomarkers on 1, 3 and 7 days after nephrotoxin administration. For renal biomarkers reflecting the value of glomerular filtration rate (creatinine in the blood, cutoff 112,77 µmol/l) the mechanism of cell death (TPA in urine, cutoff of 5.28 IU/ml), degenerative changes and regeneration (KIM-1 in urine, cutoff of 0.28 ng/ml; at values above 8,2 ng/ml the lethal effect can be expected), the inflammatory infiltration and the induction of tissue reparation (MCP-1 in urine, cutoff 11,70 pg/ml, TGF-β1 in the urine, cutoff 34,33 pg/ml), the sensitivity and specificity have been determined. According to the sequence of urine level increase, the studied biomarkers can be arranged in the following series: early stage – TPA; stage of necrosis growth and leukocyte infiltration – KIM-1, MCP-1, creatinine; stage of deep necrotic changes – TGF-β1. The studied markers are of interest for use as diagnostic tools in determining the stage of kidney disease in nephrotoxic poisoning.