D.A. Alekhina - Post-graduate Student, Laboratory of the Experimental Hygienic Studies of Scientific, Research Institute for Complex Problems of Hygiene and Occupational Diseases, Kemerovo Region, Novokuznetsk A.G. Zhukova - Dr.Sc. (Biol.), Leading Research Scientist, Laboratory of the Experimental Hygienic Studies of Scientific, Research Institute for Complex Problems of Hygiene and Occupational Diseases, Kemerovo Region, Novokuznetsk E-mail: nyura_g@mail.ru T.G. Sazontova - Dr.Sc. (Biol.), Professor, Laboratory of Adaptive Medicine, Faculty of Fundamental Medicine, M.V. Lomonosov Moscow State University E-mail: yva1950@gmail.com

Free radical oxidation and intracellular protective systems in heart, lung and liver were estimated in experimental model of sodium fluoride action (rats consumed NaF solution, 10 mg/l, during three weeks). Low dose fluoride action at the early period induces tissue specified response which has been realized by means of transcription factor HIF-1α, constitutive and inducible HSP proteins as well as enzymes of antioxidant protection. After 3 weeks of low fluoride action the level of HIF-1α, HSC73, HOx-1 and HOx-2 in heart was increased. HSP72 level increase in 4,4 times on 3 day, but on 6 day and 3 week returned to control values. Antioxidant enzymes (superoxide dismutase and catalase) activity on 3 day was 49 and 15% higher than in control, on 6 day decrease to control value, and after 3 weeks increase to 57 and 32% respectively. This high level of protective proteins is compensatory and essential for both damage effect of hypoxia and free radical oxidation development in myocardium. Indeed, amount of TBARS in heart after 3 weeks of NaF consumption was low at 3 week of experiment. A of low dose fluoride consumption the resistance of membrane structures to free radical oxidation in lung was not changed in compare with control. This compensation took place due to activation of intracellular protective systems: on 3 day of experiment HIF-1α, HSC73, HSP72 and HOx-2 levels increased significantly and was constant up to 3 week. Catalase activity increased to 3 and 6 day of fluoride consumption. In liver, in contrast to heart and lung, free radical oxidation was significantly activated on 3 day of experiment. This is due to the fact that contents of transcription factor HIF-1α, constitutive proteins HSC73, HOx-2 and inducible proteins HSP72, HOx-1 were increase. These protective proteins level and activity of free radical oxidation were decrease to control level after 6 day of experiment. High level of HIF-1α, НОх-1, НОх-2 and HSP72 was observed on 3 week; it was reason why the resistance of liver structures to free radical oxidation remain at control level. Activities of superoxide dismutase and catalase increase during first week of fluoride action and was 1.6 and 1.8 times more on 3 day and 2.6 and 2.0 times more on 6 day, respectively. Thus, on early stages of low dose fluoride consumption we have shown increase level of HIF-1α, HSP72, HSC73, HOx-1, HOx-2 and activity of antioxidant system in heart, lung and liver. Maximal activation of protective systems which characterized predominantly hypoxic component of fluoride action has been shown in liver, stressory component - in heart. Increased level of intracellular protective systems in heart and liver on early stages of fluoride action induces higher resistance of tissue structures to free radical oxidation whereas in lung preserved the resistance at control level. This activation of protective systems may consider like prognostic criteria of damage factor action. Prolongation of this factor attack may induce failure of physiological adaptive body protection and indicates necessity of occasional preventive or therapeutic procedures.

 

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