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Department of Cellular and Structural Biology and Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78284-7762
Received 25 November 1996; accepted in final form 25 March 1997.
Pablos, Marta I., Russel J. Reiter, Jin-Ing Chuang, Genaro
G. Ortiz, Juan M. Guerrero, Ewa Sewerynek, Maria T. Agapito, Daniela
Melchiorri, Richard Lawrence, and Susan M. Deneke. Acutely administered melatonin reduces oxidative damage in lung and brain induced by hyperbaric oxygen. J. Appl.
Physiol. 83(2): 354-358, 1997.
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.
free radicals; antioxidant enzymes; lipid peroxidation; pineal hormone
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