title: Effects of drugs used in endotoxic shock on oxidative stress and organ damage markers.
abstract: The aim of this study was to determine the effects of enrofloxacin (ENR), flunixin meglumine (FM) and dexamethasone (DEX) on antioxidant status and organ damage markers in experimentally-induced endotoxemia. Rats were divided into three groups. To induce endotoxemia, lipopolysaccharide (LPS) was injected into all groups, including the positive control. The two other groups received the following drugs (simultaneously with LPS): ENR + FM + low-dose DEX and ENR + FM + high-dose DEX. After the treatments, blood samples were collected at 0, 1, 2, 4, 6, 8, 12, 24 and 48 h. Oxidative stress parameters were determined by ELISA, while serum organ damage markers were measured by autoanalyser. LSP increased (p < 0.05) malondialdehyde, 13,14-dihydro-15-keto-prostaglandin F(2 alpha) and nitric oxide, while LPS reduced vitamin C. These changes were especially inhibited (p < 0.05) by ENR + FM + high-dose DEX. LPS increased organ damages markers. Cardiac and hepatic damage was not completely inhibited by any treatment, whereas renal damage was inhibited by two treatments. This study suggested that ENR + FM + high-dose DEX is most effective in the LPS-caused oxidative stress and organ damages.
authors.affiliation: Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Selcuk, 42031, Campus, Konya. eyazar@selcuk.edu.tr
authors.forename: Enver
authors.initials: E
authors.lastname: Yazar
authors.forename: Ayse
authors.initials: A
authors.lastname: Er
authors.forename: Kamil
authors.initials: K
authors.lastname: Uney
authors.forename: Aziz
authors.initials: A
authors.lastname: Bulbul
authors.forename: Gulcan Erbil
authors.initials: GE
authors.lastname: Avci
authors.forename: Muammer
authors.initials: M
authors.lastname: Elmas
authors.forename: Bunyamin
authors.initials: B
authors.lastname: Tras
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000097:blood; D001322:Autoanalysis; D015415:Biomarkers / Q000097:blood; D003002:Clonixin / Q000031:analogs & derivatives* / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D004195:Disease Models, Animal; D004359:Drug Therapy, Combination; D000077422:Enrofloxacin; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D024841:Fluoroquinolones / Q000494:pharmacology*; D006331:Heart Diseases / Q000209:etiology / Q000517:prevention & control; D007674:Kidney Diseases / Q000209:etiology / Q000517:prevention & control; D008070:Lipopolysaccharides; D008107:Liver Diseases / Q000209:etiology / Q000517:prevention & control; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009102:Multiple Organ Failure / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D009569:Nitric Oxide / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012772:Shock, Septic / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy*; D013482:Superoxide Dismutase / Q000097:blood; D013997:Time Factors
chemical_list: D015415:Biomarkers; D024841:Fluoroquinolones; D008070:Lipopolysaccharides; C440499:lipopolysaccharide, Escherichia coli O111 B4; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; D009569:Nitric Oxide; D000077422:Enrofloxacin; D008315:Malondialdehyde; D003907:Dexamethasone; C014558:flunixin meglumine; D015237:Dinoprost; D013482:Superoxide Dismutase; D001205:Ascorbic Acid; D003002:Clonixin