Mechanisms of Intracellular Defense and Activity of Free Radical Oxidation in Rat Myocardium in the Dynamics of Chronic Fluorine Intoxication

Kiseleva

et al. 2018

HAS

Introduction. Fluoride in high concentrations has a toxic effect not only on bone tissue but also on the heart, liver, kidneys, and brain. In the implementation of the response to toxic doses of fluorine the proteins of the HSP family are involved regulating intracellular and tissue homeostasis under various stress effects. The toxic effect of high fluorine concentrations the mechanisms of which are disclosed in fluorosis can be realized and at a level significantly lower than a toxic one. In the literature, there is little data on the peculiarities of the effects of low fluorine concentrations at the tissue and cellular levels. The aim of the study. To investigate the impact of low fluorine concentrations on the tissue level of HSP family proteins in the brain and liver of laboratory animals. Material and methods. The experiments were carried out on 60 white male rats of the same age weighing 200-250 g. The rats were divided into 2 groups: the control and the group of the animals exposed to sodium fluoride (NaF) within 6 weeks (at a concentration of 10 mg/l corresponding to the daily fluorine dose of 1.2 mg/kg per body weight). We determined the level of inducible HSP72 and HSP32 (heme-oxygenase-1) referred to proteins of HSP family (Heat shock proteins), the activity of free radical processes and antioxidant enzymes (superoxide dismutase (SOD) and catalase) in the brain and liver tissues. Results. The important role of stress-inducible HSP72 protein in protecting the brain from the damage caused by the prolonged exposure to low fluorine concentrations was shown. In the liver, a protective role against fluoride exposure is played by the protein HSP32 with antioxidant properties. At the tissue level, the prolongation of the terms of the development of chronic fluoride intoxication with low fluorine concentrations was revealed. In the liver appeared to be the highly sensitive organ to the fluorine accumulation, the significant lesion was detected.

Experimental Study of the Impact of Low Fluorine Concentrations on the Tissue Level of HSP Family Proteins

Kiseleva

et al. 2018

HAS

Adaptogenic correction of free radical brain damage in subchronic exposure to sodium fl uoride

Myditsina truda I promyshlennaya ekologiy

Казицкая³

et al. 2020

Introduction. Fluorine compounds in small doses, but with prolonged exposure, cause various disorders in organs at the cellular and molecular levels. Activation of free-radical processes plays an important role in the damaging eff ect of fl uorides. Th erefore, one of the most eff ective ways to limit fl uorine-induced damage is to directly aff ect free-radical processes using herbal preparations with antioxidant properties.The aim of the study is to study the eff ect of a dihydroquercetin-based drug on the activity of free radical processes in brain tissue under subchronic exposure to sodium fl uoride (NaF).Materials and methods. Th e work was performed on white male laboratory rats weighing 200-250 g. Th e rats were divided into 3 groups: 1 — control; 2 — rats with chronic exposure to sodium fl uoride (NaF) for 9 weeks; 3 — rats receiving a NAF solution with simultaneous administration of a complex drug based on dihydroquercetin at a dose of 3 mg/kg in 1% starch gel for 3, 6 and 9 weeks. The activity of free radical oxidation and antioxidant defense enzymes — superoxide dismutase (SOD) and catalase-was determined in the cerebral cortex. Th e level of expression of hypoxia-induced transcription factor HIF — 1A and inducible forms of proteins HSP72 and HSP32 were determined in the cytosolic fraction of brain tissue.Results. In the early stages of subchronic fl uoride exposure (1-3 weeks), the expression of protective proteins HIF-1α, HSP72, HSP32 and catalase was shown in the rat cortex, as a result of which the activity of free-radical processes was maintained at the control level. An increase in the timing of fl uoride intake to 9 weeks led to a decrease in antioxidant protection and signifi cant activation of free radical oxidation in brain tissue. Daily administration of a complex drug with dihydroquercetin for 3, 6 and 9 weeks to rats with subchronic fl uoride exposure led to a decrease in the severity of pro- and antioxidant balance disorders in the cerebral cortex. At the same time, the greatest protective eff ect of dihydroquercetin with fl uoride exposure was manifested by the 9th week of its administration.Conclusions. When subchronic intake of fl uorides in the body, the drug based on dihydroquercetin has a neuroprotective eff ect, which is manifested by an increase in the activity of antioxidant enzymes of fr ee radical oxidation and catalase and the resistance of the cortex to induced fr ee radical oxidation.

Experimental models of vibration disease (literature review)

Kizichenko²,

et al. 2022

Hygiene and Sanitation

Introduction. Long-term vibration exposure to the human body is a risk factor for the development of occupational diseases and comorbid conditions causing, first of all, the pathology of the nervous system, as well as the cardiovascular, gastrointestinal tract and musculoskeletal systems. Pathogenetic aspects of vibration exposure at the molecular level remain open and require the search for adequate experimental animal models. The review describes experimental methods for studying vibration disease. A literature search was conducted in the databases MedLine, PubMed, Web of Science, Scopus, Google Scholar, CyberLeninka and RSCI. The results of experimental studies differ due to the difference in frequencies and duration of vibration exposure. Sanitary and hygienic characteristics of workplaces of coal-mining enterprises in Kuzbass. Data are given at the levels of local and whole-body vibration at the workplaces of an underground sinker, a stope miner, and a mining machine operator. Experimental modelling of local and whole-body vibration. Experimental methods of vibration exposure to laboratory rats, mice and rabbits at the local and whole-body levels are described. The presented experimental models are as close as possible to real vibration effects in production conditions. Vibration at frequencies above 4 Hz has been shown to cause changes in the structure and functions of peripheral vessels and nerves, along with hypoxic damage of the brain, heart, kidneys, liver, and skeletal muscles. Conclusion. Experimental modelling of vibration disease makes it possible to study the organ-specific molecular mechanisms of damaging vibration exposure to the body and develop effective preventive and therapeutic measures.