title: Protective effects of tungstophosphoric acid and sodium tungstate on chemically induced liver necrosis in wistar rats.
abstract: OBJECTIVE
  Many chemical compounds and infectious agents such as viruses induce liver damage like necrosis or fulminant hepatic failure which is sometimes difficult to manage by medical therapies. The induced liver necrosis by carbon tetrachloride (CCl4) and thioacetamide (TAA) are exemplary models for experimental liver necrosis caused by oxygen free radicals. The aim of this study was to investigate the effects of tungstophosphoric acid (TPA) and sodium tungstate (ST) on liver injury induced by CCl4 or TAA.
  
  
  METHODS
  Hepatoprotective effects of TPA and ST on acute liver necrosis, chemically induced, were evaluated by the activity of serum enzymes (alkaline phosphatase, alanine transaminase and aspartate transaminase), oxidative stress parameters (activity of xanthine oxidase, concentrations of malondialdehyde and production of superoxide anion), antioxidative defence markers (concentration of reduced glutathione), and histopathology in Wistar rats. Liver necrosis was induced by administering a single intraperitoneal (i.p.) injection of CCl4 (1.0 ml/kg b.wt. of 80% CCl4 in corn oil) or a single i.p. injection of TAA (400 mg/kg b.w. dissolved in normal saline). TPA and ST were administrated to rats orally for 7 weeks (50 mg/kg b.wt.) prior to induction of liver necrosis.
  
  
  RESULTS
  Induced liver necrosis caused significant elevation of activity of liver enzymes, parameters of oxidative stress and marked changes in histopathology, like necrosis of hepatocytes, hepatocyte degeneration and infiltration of inflammatory cells. In TPA and ST pretreated rats histopathological changes were almost absent, serum enzymes and oxidative stress parameters were decreased, while at the same time the concentration of reduced gluthathione was increased.
  
  
  CONCLUSIONS
  The present findings suggest that treatment with TPA and ST for 7 weeks could be useful for the prevention of hepatic injury in rats.
authors.affiliation: Department of Analytical Chemistry, Faculty of Pharmacy, University of Belgrade, Serbia. snezaum@pharmacy.bg.ac.yu
authors.forename: Snezana
authors.initials: S
authors.lastname: Uskoković-Marković
authors.forename: Marina
authors.initials: M
authors.lastname: Milenković
authors.forename: Aleksandra
authors.initials: A
authors.lastname: Topić
authors.forename: Jelena
authors.initials: J
authors.lastname: Kotur-Stevuljević
authors.forename: Aleksandra
authors.initials: A
authors.lastname: Stefanović
authors.forename: Jelena
authors.initials: J
authors.lastname: Antić-Stanković
mesh_terms: D000208:Acute Disease; D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002251:Carbon Tetrachloride; D004195:Disease Models, Animal; D005260:Female; D005978:Glutathione / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000473:pathology*; D008111:Liver Function Tests; D009336:Necrosis / Q000139:chemically induced / Q000188:drug therapy / Q000503:physiopathology; D018384:Oxidative Stress / Q000187:drug effects; D010756:Phosphoric Acids / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013853:Thioacetamide; D017973:Tungsten Compounds / Q000494:pharmacology*
chemical_list: C519880:12-tungstophosphoric acid; D000975:Antioxidants; D010756:Phosphoric Acids; D017973:Tungsten Compounds; D013853:Thioacetamide; C025399:sodium tungstate(VI); D002251:Carbon Tetrachloride; D005978:Glutathione