RESUMEN
Arsenazo III (AIII) (100 mg/kg ip in saline) administration to Sprague-Dawley male rats 30 min before or 6 or 10 hr after CCl4 [1 ml/kg ip as a 20% (v/v) solution in olive oil] significantly prevented liver necrosis but not fatty liver caused by the hepatotoxin at 24 hr as demonstrated either by histology or by determination of isocitric acid dehydrogenase in plasma. AIII did not modify the CCl4 concentrations reaching the liver, the intensity of the covalent binding of CCl4-reactive metabolites to hepatic microsomal lipids, or the CCl4-promoted lipid peroxidation process at either 1 or 3 hr of poisoning. AIII administration enhanced glutathione (GSH) levels in liver and significantly prevented the CCl4-induced minor decreases in GSH content and the CCl4-induced increases in calcium content at 24 hr of intoxication. AIII treatment further enhanced the CCl4-induced decreases in body temperature of the poisoned rats. Results suggest that AIII's preventive effects might be related to its very well-known calcium-chelating properties, but that additional factors related to AIII's ability to increase GSH content in liver or to decrease body temperature of CCl4-intoxicated animals may also play a role.
Asunto(s)
Arsenazo III/farmacología , Calcio/metabolismo , Intoxicación por Tetracloruro de Carbono/prevención & control , Tetracloruro de Carbono/toxicidad , Hígado/patología , Microsomas Hepáticos/metabolismo , Animales , Tetracloruro de Carbono/metabolismo , Intoxicación por Tetracloruro de Carbono/sangre , Glutatión/metabolismo , Isocitrato Deshidrogenasa/sangre , Peroxidación de Lípido/efectos de los fármacos , Hígado/efectos de los fármacos , Hígado/metabolismo , Masculino , Microsomas Hepáticos/efectos de los fármacos , Microsomas Hepáticos/enzimología , Necrosis , Ratas , Ratas Sprague-DawleyRESUMEN
Environmental (b2) and genetic heritability (h2) of serum isocitrate dehydrogenase (ICDH) were estimated in 96 pairs of healthy twins according to a path analysis model. The results showed significant heritability (0.42) and a very low environmental component (based on obesity and level of habitual physical activity), suggesting that these factors do not influence ICDH serum activity.
Asunto(s)
Isocitrato Deshidrogenasa/genética , Gemelos/genética , Adulto , Creatina Quinasa/sangre , Creatina Quinasa/genética , Ambiente , Femenino , Humanos , Isocitrato Deshidrogenasa/sangre , Masculino , Modelos Genéticos , Piruvato Quinasa/sangre , Piruvato Quinasa/genética , Gemelos Dicigóticos/genética , Gemelos Monocigóticos/genéticaAsunto(s)
Proteínas Sanguíneas/análisis , Eritrocitos/enzimología , Indígenas Sudamericanos , Adenosina Monofosfato , Brasil , Ceruloplasmina/análisis , Electroforesis en Gel de Poliacrilamida , Electroforesis en Gel de Almidón , Femenino , Frecuencia de los Genes , Variación Genética , Geografía , Glucosa-6-Fosfato Isomerasa/sangre , Guyana , Humanos , Isocitrato Deshidrogenasa/sangre , Masculino , Linaje , Péptido Hidrolasas/sangre , Fosfotransferasas/sangre , Polimorfismo Genético , Albúmina Sérica/análisis , VenezuelaRESUMEN
Serum glutamic-pyruvic-transaminase, isocitric-dehydrogenase, and bilrubin were measured in malnourished children. Greatly increased levels were found in chlidren who died later. Clinical observations suggest that with modern treatment childern with severe malnutrition survive unless they have hepatic failure. There was no difference in enzyme distribution between the groups of children with marasmus and those with kwashiorkor. It is suggested that leakage of enzymes from liver cells may lead to failure of liver function. Measurements of the enzyme content of some liver-biopsy specimens support this argument (AU)