RESUMO
The authors studied intracellular liver protective mechanisms in development of chronic fluorine intoxication. Findings are that synthesis of protective proteins HIF-1α, HOx-1, HOx-2 and HSP72, restricting free radical oxidation in hepatocytes increased in liver at early stages (1-3 weeks) of exposure to fluorine. At late terms of chronic fluorine intoxication (6-12 weeks), damaging effects of fluorine result from its genotixicity - ability to suppress synthesis of intracellular protective proteins and enzymes of main metabolic cycles in liver.
Assuntos
Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Hepatócitos/metabolismo , Fígado/metabolismo , Biossíntese de Proteínas/efeitos dos fármacos , Fluoreto de Sódio/toxicidade , Animais , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Masculino , RatosRESUMO
The mechanisms of intracellular defense and activity of free radical oxidation in the myocardium were studied in the dynamics of chronic fluorine intoxication. At the early stages of fluorine intoxication (day 3-week 3), the concentrations of defense proteins HIF-1α, HSC73, and HOx-2 and activity of the main metabolic enzymes increased, which promoted maintenance of cardiomyocyte structure and function at the normal physiological level. At late stages of fluorine intoxication (weeks 6 and 9), metabolic changes in the myocardium attest to high strain of the adaptive mechanisms.