RESUMO
Oxidative stress associated with the presence of elevated concentrations of ammonia in the brain has been proposed as one possible mechanism involved in ammonia toxicity. In a previous study [Brain Res.973 (2003) 31], we reported that neonatal rats are more resistant to acute ammonia toxicity than adult rats. In the present work, we studied the antioxidant status of the brain in hyperammonemic neonatal rats. Increased activities of the antioxidant enzymes and enhanced glutathione content were found in the brains of the hyperammonemic neonatal rats as compared to the controls. In addition, no changes in brain reactive oxygen species (ROS) levels and lipid peroxidation due to hyperammonemia were found. Therefore, acute ammonia intoxication does not induce oxidative stress in neonatal rats, a fact that may explain the resistance against hyperammonemia shown by neonatal rats.
Assuntos
Amônia/toxicidade , Antioxidantes/uso terapêutico , Encéfalo/enzimologia , Hiperamonemia/prevenção & controle , Animais , Animais Recém-Nascidos , Catalase/metabolismo , Glutationa/metabolismo , Dissulfeto de Glutationa/metabolismo , Hiperamonemia/induzido quimicamente , Hiperamonemia/enzimologia , Peroxidases/metabolismo , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismoRESUMO
The aim of the present work was to study the effects of hyperammonemia on brain energy metabolism in neonatal rats. Rats were rendered hyperammonemic by ammonium acetate administration. This decreased brain ATP concentrations but enhanced brain ammonia and lactate levels in both adult and neonatal rats. In adult rats, the decrease in brain ATP concentrations was accompanied by a plunge in the respiratory control rate (RCR) of brain mitochondria. However, the ammonia-induced effect on RCR was not observed in neonatal rats, suggesting that the fall in ATP levels observed in neonatal rats would not be due to an impairment of mitochondrial respiratory efficiency. However, in neonatal rats the increase in blood and brain ammonia concentrations did not change brain glutamate concentrations but decreased glutamine contents. These results may be of relevance for the understanding of the resistance of neonatal rats observed in this work to acute ammonia toxicity
Assuntos
Encéfalo/metabolismo , Hiperamonemia/metabolismo , Doença Aguda , Trifosfato de Adenosina/metabolismo , Fatores Etários , Amônia/metabolismo , Amônia/toxicidade , Animais , Animais Recém-Nascidos , Encéfalo/efeitos dos fármacos , Feminino , Ácido Glutâmico/metabolismo , Hiperamonemia/induzido quimicamente , Ácido Láctico/metabolismo , Masculino , Ratos , Ratos WistarRESUMO
Mitochondria play an essential role in the generation of the energy needed for eukaryotic cell life and in the release of molecules involved in initiation of cell death. Here we review the changes in isolated mitochondrial fluorescent populations as distinguished by flow cytometry during postnatal development and their regulation by thyroid hormones and catecholamines. The use of flow cytometry in the study of mitochondrial changes occurring under hypothyroidism, alcohol abuse and aging is also reviewed.