Glutathione Ethyl Ester Supplementation Prevents Mortality in Newborn Rats Exposed to Hyperoxia
Autor: | Rakesh K. Singhal, Ajey Jain |
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Rok vydání: | 2000 |
Předmět: |
Time Factors
Antioxidant medicine.medical_treatment chemistry.chemical_element Hyperoxia Pharmacology medicine.disease_cause Oxygen Rats Sprague-Dawley chemistry.chemical_compound medicine Glutathione ethyl ester Animals Lung Respiratory distress business.industry Glutathione Immature lungs Rats Microscopy Electron Animals Newborn chemistry Biochemistry Pediatrics Perinatology and Child Health medicine.symptom business Oxidative stress Follow-Up Studies Developmental Biology |
Zdroj: | Neonatology. 77:261-266 |
ISSN: | 1661-7819 1661-7800 |
Popis: | Human premature neonates suffer from respiratory distress syndrome due to immature lungs and require assisted ventilation with high concentrations of oxygen. Hyperoxic exposure and/or antioxidant deficiency causes an increase in the lung levels of reactive oxygen species (ROS) leading to oxidative stress-induced cellular damage. In this study, we explored the protective role of the nonenzymatic antioxidant glutathione, by administering glutathione ethyl ester (GSHEE), in newborn rats exposed to hyperoxia (>95% FiO2). Our results show that GSHEE supplementation (5 mmol/kg/day) prevents mortality in newborn rats exposed to hyperoxia. We further show that delayed GSHEE supplementation in newborn rats, pre-exposed to hyperoxia for 4 days, also prevents death. Electron microscopic studies on the lung of GSHEE-treated hyperoxic rats showed normal histology and an absence of the marked swelling and degeneration of mitochondria and lamellar bodies, which are typically observed in the hyperoxic lungs of newborn rats. Furthermore, there were no apparent differences in weight gain or general appearance/activity among room air and hyperoxic GSHEE-supplemented animals when monitored, post-treatment, in room air for 30 days. Our results show a preventive/therapeutic role of GSHEE supplementation against mortality caused in newborn rats due to hyperoxic exposure, and may further be applicable to a variety of degenerative diseases that are caused as a result of ROS accumulation. |
Databáze: | OpenAIRE |
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