title: Oxidative preconditioning affords protection against carbon tetrachloride-induced glycogen depletion and oxidative stress in rats.
abstract: The rectal insufflation of a judicious dose of ozone, selected from that used in clinical practice, is able to promote oxidative preconditioning or oxidative stress tolerance preventing the hepatocellular damage mediated by free radicals. In order to evaluate the effects of ozone oxidative preconditioning on carbon tetrachloride-mediated hepatotoxicity, the following experimental protocol was designed: group 1 (negative control, sunflower oil i.p.); group 2 (CCl(4) in sunflower oil, 1 ml kg(-1) i.p.); group 3 (15 ozone-oxygen pretreatments at a dose of 1 mg kg(-1) via rectal insufflation + CCl(4) as in group 2); group 4 (ozone control group, 15 ozone-oxygen pretreatments + sunflower oil i.p.). Ozone pretreatment prevented glycogen depletion (as demonstrated by biochemical and histopathological findings) and avoided lactate overproduction associated with the hepatotoxic effects of CCl(4). The administration of CCl(4) increased lipid peroxidation (as measured by thiobarbituric acid-reactive substances) and uric acid levels and inhibited superoxide dismutase activity. All these deleterious effects induced by CCl(4) were prevented by ozone pretreatment. The administration of ozone without CCl(4) (ozone control group) did not produce any changes in the evaluated parameters. Our results showed that ozone treatment, in our experimental conditions, was able to prevent anaerobic glycolysis and oxidative stress induced by CCl(4).
authors.affiliation: Center for Research and Biological Evaluation, University of Havana, Institute of Pharmacy and Food Sciences, Apartado Postal 6079, Havana City 10600, Cuba. ecjalil@cieb.sld.cu
authors.forename: E
authors.initials: E
authors.lastname: Candelario-Jalil
authors.forename: S
authors.initials: S
authors.lastname: Mohammed-Al-Dalain
authors.forename: O S
authors.initials: OS
authors.lastname: Fernández
authors.forename: S
authors.initials: S
authors.lastname: Menéndez
authors.forename: G
authors.initials: G
authors.lastname: Pérez-Davison
authors.forename: N
authors.initials: N
authors.lastname: Merino
authors.forename: S
authors.initials: S
authors.lastname: Sam
authors.forename: H H
authors.initials: HH
authors.lastname: Ajamieh
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001835:Body Weight / Q000187:drug effects; D002252:Carbon Tetrachloride Poisoning / Q000188:drug therapy / Q000517:prevention & control*; D002374:Catalase / Q000032:analysis; D005260:Female; D016166:Free Radical Scavengers / Q000037:antagonists & inhibitors; D006003:Glycogen / Q000172:deficiency*; D006019:Glycolysis / Q000187:drug effects; D007274:Injections, Intraperitoneal; D007327:Insufflation; D019344:Lactic Acid / Q000032:analysis; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D010126:Ozone / Q000008:administration & dosage / Q000494:pharmacology*; D011506:Proteins / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000032:analysis; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014527:Uric Acid / Q000032:analysis
chemical_list: D000975:Antioxidants; D016166:Free Radical Scavengers; D011506:Proteins; D017392:Thiobarbituric Acid Reactive Substances; D014527:Uric Acid; D019344:Lactic Acid; D010126:Ozone; D006003:Glycogen; D002374:Catalase; D013482:Superoxide Dismutase