Acutely administered melatonin reduces oxidative damage in lung and brain induced by hyperbaric oxygen

M. I. Pablos, R. J. Reiter, J. I. Chuang, G. G. Ortiz, J. M. Guerrero, E. Sewerynek, M. T. Agapito, D. Melchiorri, R. Lawrence, S. M. Deneke

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101 引文 斯高帕斯(Scopus)

摘要

Hyperbaric oxygen exposure rapidly induces lipid peroxidation and cellular damage in a variety of organs. In this study, we demonstrate that the exposure of rats to 4 atmospheres of 100% oxygen for 90 min is associated with increased levels of lipid peroxidation products [malonaldehyde (MDA) and 4-hydroxyalkenals (4-HDA)] and with changes in the activities of two antioxidative enzymes [glutathione peroxidase (GPX) and glutathione reductase (GR)], as well as in the glutathione status in the lungs and in the brain. Products of lipid peroxidation increased after hyperbaric hyperoxia, both GPX and GR activities were decreased, and levels of total glutathione (reduced+oxidized) and glutathione disulfide (oxidized glutathione) increased in both lung and brain areas (cerebral cortex, hippocampus, hypothalamus, striatum, and cerebellum) but not in liver. When animals were injected with melatonin (10 mg/kg) immediately before the 90-min hyperbaric oxygen exposure, all measurements of oxidative damage were prevented and were similar to those in untreated control animals. Melatonin's actions may be related to a variety of mechanisms, some of which remain to be identified, including its ability to directly scavenge free radicals and its induction of antioxidative enzymes via specific melatonin receptors.

原文English
頁(從 - 到)354-358
頁數5
期刊Journal of Applied Physiology
83
發行號2
DOIs
出版狀態Published - 1997 一月 1

All Science Journal Classification (ASJC) codes

  • 生理學
  • 生理學(醫學)

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