Effects of acute and chronic administration of methylprednisolone on oxidative stress in rat lungs.

OBJECTIVE: To determine the effects of acute and chronic administration of methylprednisolone on oxidative stress, as quantified by measuring lipid peroxidation (LPO) and total reactive antioxidant potential (TRAP), in rat lungs. METHODS: Forty Wistar rats were divided into four groups: acute treatment, comprising rats receiving a single injection of methylprednisolone (50 mg/kg i.p.); acute control, comprising rats i.p. injected with saline; chronic treatment, comprising rats receiving methylprednisolone in drinking water (6 mg/kg per day for 30 days); and chronic control, comprising rats receiving normal drinking water. RESULTS: The levels of TRAP were significantly higher in the acute treatment group rats than in the acute control rats, suggesting an improvement in the pulmonary defenses of the former. The levels of lung LPO were significantly higher in the chronic treatment group rats than in the chronic control rats, indicating oxidative damage in the lung tissue of the former. CONCLUSIONS: Our results suggest that the acute use of corticosteroids is beneficial to lung tissue, whereas their chronic use is not. The chronic use of methylprednisolone appears to increase lung LPO levels.

Effects of acute and chronic administration of methylprednisolone on oxidative stress in rat lungs / Efeitos da administração aguda e crônica de metilprednisolona no estresse oxidativo em pulmões de ratos

Objective: To determine the effects of acute and chronic administration of methylprednisolone on oxidative stress, as quantified by measuring lipid peroxidation (LPO) and total reactive antioxidant potential (TRAP), in rat lungs. Methods: Forty Wistar rats were divided into four groups: acute treatment, comprising rats receiving a single injection of methylprednisolone (50 mg/kg i.p.); acute control, comprising rats i.p. injected with saline; chronic treatment, comprising rats receiving methylprednisolone in drinking water (6 mg/kg per day for 30 days); and chronic control, comprising rats receiving normal drinking water. Results: The levels of TRAP were significantly higher in the acute treatment group rats than in the acute control rats, suggesting an improvement in the pulmonary defenses of the former. The levels of lung LPO were significantly higher in the chronic treatment group rats than in the chronic control rats, indicating oxidative damage in the lung tissue of the former. Conclusions: Our results suggest that the acute use of corticosteroids is beneficial to lung tissue, whereas their chronic use is not. The chronic use of methylprednisolone appears to increase lung LPO levels. .

Objetivo: Determinar os efeitos da administração aguda e crônica de metilprednisolona no estresse oxidativo, por meio da quantificação da peroxidação lipídica (POL) e do potencial antioxidante reativo total (PART), em pulmões de ratos. Métodos: Quarenta ratos Wistar foram divididos em quatro grupos: tratamento agudo, com ratos recebendo uma dose única de metilprednisolona (50 mg/kg i.p.); controle agudo, com ratos recebendo injeção unida de salina; tratamento crônico, com ratos recebendo metilprednisolona v.o. na água do bebedouro (6 mg/kg por dia durante 30 dias; e controle crônico, com ratos recebendo água de bebedouro normal). Resultados: Os níveis de PART foram significativamente maiores no grupo tratamento agudo que no grupo controle agudo, sugerindo uma melhora do sistema de defesa pulmonar. Os níveis de POL foram significativamente maiores no grupo tratamento crônico que no grupo controle crônico, indicando dano oxidativo no tecido pulmonar. Conclusões: Nossos resultados sugerem que o uso agudo de corticoides foi benéfico aos tecidos pulmonares, enquanto seu uso crônico não o foi. O uso crônico de metilprednisolona parece aumentar os níveis pulmonares da POL. .

Effect of systemically administered low potassium dextran solution on oxidative stress in a rat model of lung ischemia.

Systemic administration of the low-potassium dextran solution on the peripheral oxidative stress was evaluated in an animal model of lung ischemia-reperfusion in rats. In one experiment, male Wistar rats were divided into two groups (n=5): one received intravenous saline, whereas in the other the animals were given intravenous low potassium dextran solution. In another experiment, male Wistar rats were divided into four groups (n=5): control, ischemia, saline and low potassium dextran. Except for the control animals, all groups were submitted to left hilar clamping for 30 min, followed by reperfusion for 30 min. Saline or low potassium dextran was administered intravenously immediately before clamp removal. In the first experiment there were no significant differences in lipid peroxidation. Total radical trapping potential measurements showed a significant increase in animals receiving low potassium dextran; in the second experiment, there was an increase in lipid peroxidation in both saline and ischemia groups compared to controls, and low potassium dextran. Low potassium dextran group showed an increase in total radical trapping potential measurements compared to all other groups. Ischemia-reperfusion injury mediated by reactive oxygen species was attenuated by the systemic use of low potassium dextran in this animal model of ischemia-reperfusion of the lung.