title: Chronic hyperbaric oxygen treatment elicits an anti-oxidant response and attenuates atherosclerosis in apoE knockout mice.
abstract: We previously demonstrated that hyperbaric oxygen (HBO) treatment inhibits diet-induced atherosclerosis in New Zealand White rabbits. In the present study we investigate the mechanisms that might be involved in the athero-protective effect of HBO treatment in a well-accepted model of atherosclerosis, the apoE knockout (KO) mouse. We examine the effects of daily HBO treatment (for 5 and 10 weeks) on the components of the anti-oxidant defense mechanism and the redox state in blood, liver and aortic tissues and compare them to those of untreated apoE KO mice. HBO treatment results in a significant reduction of aortic cholesterol content and decreased fatty streak formation. These changes are accompanied by a significant reduction of autoantibodies against oxidatively modified LDL and profound changes in the redox state of the liver and aortic tissues. A 10-week treatment significantly reduces hepatic levels of TBARS and oxidized glutathione, while significantly increases the levels of reduced glutathione, glutathione reductase (GR), transferase, Se-dependent glutathione peroxidase and catalase (CAT). The effects of HBO treatment are similar in the aortic tissues. These observations provide evidence that HBO treatment has a powerful effect on the redox state of relevant tissues and produces an environment that inhibits oxidation. The anti-oxidant response may be the key to the anti-atherogenic effect of HBO treatment.
authors.affiliation: Department of Molecular Biology & Immunology, The University of North Texas Health Science Center, Fort Worth, TX 76104, USA.
authors.forename: Bhalchandra J
authors.initials: BJ
authors.lastname: Kudchodkar
authors.forename: Anson
authors.initials: A
authors.lastname: Pierce
authors.forename: Ladislav
authors.initials: L
authors.lastname: Dory
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001013:Aorta, Thoracic / Q000473:pathology; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D043303:Aryldialkylphosphatase / Q000097:blood; D050197:Atherosclerosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D001323:Autoantibodies / Q000097:blood; D002784:Cholesterol / Q000097:blood; D005260:Female; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D006931:Hyperbaric Oxygenation; D015227:Lipid Peroxidation; D008077:Lipoproteins, LDL / Q000276:immunology; D008099:Liver / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D011817:Rabbits; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001057:Apolipoproteins E; D001323:Autoantibodies; D008077:Lipoproteins, LDL; D017392:Thiobarbituric Acid Reactive Substances; C099252:oxidized low density lipoprotein; D002784:Cholesterol; D043303:Aryldialkylphosphatase; D005978:Glutathione; D019803:Glutathione Disulfide