RESUMO
L-Dopa has now undoubtly proved itself the drug of choice in the vast majority of cases of Parkinson's Disease. When used in combination with a decarboxylase inhibitor it would appear that significant therapeutic advantages are gained (Lancet 5th May, 1973, Marsden et al 1973). The metabolism, use and side effects of L-Dopa are outlined and the role of other forms of treatment discussed (AU)
Assuntos
Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Doença de Parkinson/tratamento farmacológico , Carboxiliases/antagonistas & inibidores , Di-Hidroxifenilalanina/efeitos adversos , Di-Hidroxifenilalanina/metabolismo , Di-Hidroxifenilalanina/uso terapêutico , Doença de Parkinson/fisiopatologiaRESUMO
The kinetics of the induction of rat kidney phosphoenolpyruvate carboxykinase activity after triamcinolone and ammonium chloride administration have been investigated with a view to the further differentiation of the two processes. The half-life of kidney phosphoenolpyruvate carboxykinase activity, as measured from the decay curve after a single dose of triamcinolone, is approximately 1.4 hr. This compares with a half-life for the enzyme from acidotic kidney of approximately 3.4 hr. Analysis of the data indicates that the induction of phosphoenolpyruvate carboxykinase activity by triamcinolone may be attributed to an increase in de novo protein synthesis. Induction by acidosis is qualitatively distinct and is partly attributed to a reduction in the rate of decay of phosphoenolpyruvate carboxykinase activity. The activities of the gluconeogenic enzymes glucose-6-phosphotase, fructose-1,6-diphosphotase and phosphoenolpyruvate carboxykinase in both liver and kidney have been measured in animals separately treated with triamcinolone and ammonium chloride. Triamcinolone significantly increases the activities of liver phosphoenolpyruvate carboxykinase, kidney glucose-6-phosphatase, and kidney phosphoenolpyruvate carboxykinase only; ammonium chloride stimulates a 200 percent increase in kidney phosphoenolpyruvate carboxykinase, but has no effect on the other enzymes. The induction processes whereby triamcinolone increases phosphoenolpyruvate carboxykinase activities in liver and kidney differ qauntitatively. (AU
Assuntos
Ratos , 21003 , Masculino , Acidose/enzimologia , Cloreto de Amônio , Carboxiliases/metabolismo , Rim/enzimologia , Triancinolona Acetonida/farmacologia , Acidose/classificação , Adrenalectomia , Cloreto de Amônio/administração & dosagem , Cloreto de Amônio/farmacologia , Indução Enzimática , Frutose-Bifosfatase/análise , Glucose-6-Fosfatase/análise , Injeções Intramusculares , Injeções Intraperitoneais , Córtex Renal/enzimologia , Fígado/enzimologia , /metabolismo , Fatores de Tempo , Triancinolona Acetonida/administração & dosagemRESUMO
A method for the assay of phosphoenolpyruvate carboxykinase is presented, based on the enzymic determination of the phosphoenolpyruvate produced by the enzyme reaction. The subcellular distribution of phosphoenolpyruvate carboxykinase in the kidney of several animal species resembled the distribution in the liver. The rise in enzyme activity in the kidney cortex of rats made acidotic by feeding with ammonium chloride was not prevented by the administration of ethionine or actinomycin. The possibility is suggested that in the kidney acidosis causes activation of an inactive form of the enzyme already present. (AU)
