A.G. Zhukova, E.V. Ulanova, D.A. Shcherbakova, T.K. Yadykina

Long exposure to high fluorine concentrations on rats was accompanied by different directed change in the level of stressor blood hormones - ACTH, cortisol, and adrenaline. The similar hormonal response was directed to the onset of compensatory mechanisms and activation of metabolic cell processes: ALAT, AAT, AlP, CPK activity changed. So ALAT and AlP passed through two waves of activation - in 3 weeks of fluoric intoxication they exceeded the control level by 24 % and 13 %, in 6 weeks they decreased, and in 9 weeks new increase was registered (by 41 % and 21 % accordingly). Only in 3 weeks of fluoric intoxication CPK activity increased by 53 %. On the 12-th week of fluoric intoxication ALAT, AlP, CPK activity didn-t reliably differ from the control values. Increase in the activity of these enzymes promoted functioning glucose-alanine shunt and it was directed to involving of phosphates into bioenergy processes and stimulation of oxidative phosphorylation in mitochondrions. Besides increase in CPK activity also testified development of stress-reaction which proceeded with ATP expenditure. AAT activity decreased progressively from the 3-rd week till the 6-th one and it raised on the 9-th and 12-th weeks of fluoric priming that evidenced activation of Krebs cycle. Correlation interrelations between the change of hormone level and enzyme activity in blood of experimental rats were revealed. We observed positive correlation connection between ACTH and ALAT, ACTH and AlP levels (r = 0,873; p  0,001), between cortisol and AAT levels (r = 0,869; p  0,001). Negative correlation connection between adrenaline and AAT levels (r = -0,87; p  0,001), between adrenaline and ALAT levels (r = -0,8; p  0,01) was detected. Thus long exposure to fluorine is the stressor for an organism and is accompanied by activation of compensatory and adaptive mechanisms which promote maintenance of basic homeostatic blood indices at the physiological level. There is change in the activity of bioenergy systems both at tissue level and at organ one. At early stages of fluoric intoxication (1-3 weeks) gluconeogenesis and glucose transport intensify due to its dephosphorylation, oxidative phosphorylation in mitochondrions and synthesis of the proteins participating in these processes are activated. When increasing terms of priming with fluorine (6-9 weeks) compensatory response becomes prolonged in time and proceeds on other metabolic ways: glycolysis and Krebs cycle are activated. Chronic exposure to high fluorine concentrations (the 12-th week of fluoric priming) exhausts compensatory and adaptive mechanisms, as a result fluorosis develops, and as a whole it can be characterized as impossibility of metabolic balance.