ACUTELY ADMINISTERED MELATONIN REDUCES OXIDATIVE DAMAGE IN LUNG AND BRAIN INDUCED BY HYPERBARIC-OXYGEN

Hyperbaric oxygen exposure rapidly induces lipid peroxidation and cell ular 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 as sociated with increased levels of lipid peroxidation products [malonal dehyde (MDA) and 4-hydroxyalkenals (4-HDA)] and with changes in the ac tivities of two antioxidative enzymes [glutathione peroxidase (GPX) an d 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 area s (cerebral cortex, hippocampus, hypothalamus, striatum, and cerebellu m) but not in liver. When animals were injected with melatonin (10 mg/ kg) immediately before the 90-min hyperbaric oxygen exposure, all meas urements 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, includin g its ability to directly scavenge free radicals and its induction of antioxidative enzymes via specific melatonin receptors.