RESUMO
O objetivo foi verificar a influência da deficiência dos hormônios tireoideanos induzida por propiltiouracil (PTU) na mucosa gengival do rato, analisando bioquimicamente as proteínas totais, colágeno (hidroxiprolina) e população celular (DNA). Foram utilizados 50 ratos machos da cepa Sprague-Dawley, separados em 2 grupos: propiltiouracil (PTU) (10 mg/d i.p.), e controle (C), durante 10 semanas. As proteínas totais foram determinadas pelo método de Lowry, a hidroxiprolina pelo método de Newman e DNA pelo método de Burton. Observou-se diminuição das proteínas totais no grupo PTU (PTU= 41,23 ± 24,05; C= 63,36 ± 18,05); não houve diferença na hidroxiprolina e DNA (PTU= 2,18 ± 1,48; C= 2,29 ± 1,51) e (PTU= 0,33 ± 0,19; C= 0,46 ± 0,31). Conclui-se que o tratamento com PTU diminui o conteúdo de proteínas totais na mucosa gengival do rato, provavelmente pela diminuição da síntese protéica, sem alteração do colágeno e da população celular.
This work aimed at verifying the influence of propilthiouracil (PTU)-induced thyroid hormone deficiency on gingival mucosa of young male rats, measuring total protein concentration, collagen content and DNA concentration as indices of cellular population. Fifty Sprague-Dawley rats were used. The animals were grouped in: PTU-treated (i.p. 10 mg/d) and control rats (C). The experience was maintained for a period of 10 weeks. Total protein content of gingival mucosa tissue was determined by the Lowry method; hydroxyprolin rate, as prototype aminoacid of collagen, was determined using the Newman method, and DNA concentration was measured by Burton's methodology. The results showed decreased amounts of PTU-treated rats gingival total protein content (PTU= 41.23 ± 24.05 vs. C= 63.36 ± 18.05); no alterations were seen in hydroxyprolin concentration neither in DNA content of PTU treated rats, respectively (PTU= 2.18 ± 1.48 vs. C= 2.29 ± 1.51) and (PTU= 0.33 ± 0.19 vs. C= 0.46 ± 0.41). Thus, PTU treatment promotes a decrease in total protein content of rat gingival mucosa that may be interpreted as a decrease in protein synthesis induced by the hypothyroid condition, but with no alteration either in collagen or nucleic acid rates.
Assuntos
Animais , Masculino , Ratos , Antitireóideos/farmacologia , Colágeno/análise , Gengiva/química , Hipotireoidismo/induzido quimicamente , Propiltiouracila/farmacologia , Proteínas/análise , Antitireóideos/metabolismo , Colorimetria , Colágeno/efeitos dos fármacos , Colágeno/metabolismo , Modelos Animais de Doenças , DNA , Hidroxiprolina/análise , Propiltiouracila/metabolismo , Proteínas/efeitos dos fármacos , Proteínas/metabolismo , Ratos Sprague-Dawley , Espectrofotometria , Tiroxina/biossíntese , Tiroxina/sangue , Tri-Iodotironina/biossíntese , Tri-Iodotironina/sangueRESUMO
BACKGROUND & OBJECTIVES: Di (2-ethyl hexyl) phthalate (DEHP), a plasticizer commonly used in PVC blood storage bags leaches out in significant amounts into blood during storage. In view of many reports on the toxicity of this compound, it was considered necessary to investigate the effect of DEHP at the low level solubilized in blood on some important hormones in rats and in human blood stored in DEHP plasticized blood bags. METHODS: Rats were administered DEHP at a low level of 750 microg/100 g body weight on alternate days for 14 days. Changes in the serum insulin, blood glucose, liver glycogen level and T3, T4 and thyroid stimulating hormone (TSH) as well as cortisol in the serum were studied. Changes in the hormones were also studied in blood stored in DEHP plasticized PVC bags. RESULTS: The results indicated decrease in serum insulin, cortisol and liver glycogen, and increase in blood glucose, serum T3 and T4 in rats receiving DEHP. These changes were reversed when administration of DEHP was stopped. Similar changes in hormones were also observed in the blood stored in DEHP plasticized blood bags. INTERPRETATION & CONCLUSION: The results indicated that administration of DEHP at low levels to rats caused symptoms of diabetes, thyroid and adrenocortical dysfunction. Though the results obtained in rats cannnot be extrapolated to human, the fact that similar hormonal changes seen in human blood stored in DEHP plasticized blood bags may suggest possibility of DEHP causing similar changes in human. The fact that these changes were reversed in rats when DEHP administration was stopped, indicates that transfusion of a few units of blood to a recipient may not be harmful, but it may pose a problem during repeated transfusions such as in thalassaemia patients.
Assuntos
Animais , Glicemia/biossíntese , Preservação de Sangue/métodos , Transfusão de Sangue/métodos , Dietilexilftalato/farmacologia , Feminino , Vidro , Glicogênio/biossíntese , Hormônios/metabolismo , Humanos , Insulina/sangue , Fígado/metabolismo , Plastificantes/química , Cloreto de Polivinila/química , Ratos , Tireotropina/biossíntese , Tiroxina/biossíntese , Fatores de Tempo , Tri-Iodotironina/biossínteseRESUMO
El presente trabajo estudió la conversión de titoxina (T4) a triiodotironina (T3) en el miocardio e hígado de ratas tratadas con la droga antiarrítmica amiodarona. Ratas Wistar de 200 g de peso fueron inyectadas con amiodarona 2,5 mg/100 g de peso, ip, diariamente durante 12 días, o con la droga inhibidora de la deiodinación de T4, el ácido iopanoico (IOP) 5 mg/100 g de peso, ip, cada 12 horas durante 72 horas. Posteriormente, el corazón e hígado de cada animal fueron homogeneizados en buffer Krebs-Ringer fosfato, pH 7,4 (1:4). Alíucotas de 400 micronl de homogenato fueron separadas y se agregó ditiotreitol 8 mM y 10**-2 micronCi de 125I-T3. Para los estudios in vitro de animales no trtados, se agregó a los homogenatos, además, amiodarona 0,1 mM o IOP 10 mM. Los viales se incubaron por 2 horas a 37-C y se hizo cromatografía en alcohol amílico terciario: hexano: amonio (5:1:6). La producción de T3 en el miocardio e hígado de los grupos tratados con amiodarona o IOP descendió significativamente respecto de los controles, mientras que en los estudios in vitro la amiodarona no tuvo efecto sobre la deiodinación de T4 y el IOP bajó significativamente la conversión de T4 a T3. La degradación de T3 no fue alterada por ninguna de las dos drogas en ninguno de los dos tejidos. La amiodarona descendió signifcativamente la tirotrofina y la T3 séricas, mientras que aumentó significativamente la T4 sérica. el IOP tuvo el mismo efecto sobre la T4 y T3, pero aumentó significativamente la TSH circulante. Se concluye que el bloqueo de la producción miocárdica de T3 inducido por la amiodarona no sería el responsable de su acción antiarrítmica