title: Effect of tumor necrosis factor on hepatic oxidative stress and antioxidant defense indices in normal and Plasmodium yeolii nigeriensis infected mice.
abstract: BACKGROUND
  Plasmodium yoelii nigeriensis (P. y. nigeriensis) produces lethal malaria infection in Swiss albino mice. Reactive oxygen species (ROS) such as superoxide anion, hydrogen peroxide along with endogenously produced tumor necrosis factor (TNF) have been implicated in the pathogenesis of malaria.
  
  
  OBJECTIVE
  Study the effect of TNF on hepatic oxidative stress and antioxidant defense indices in normal and P. y. nigeriensis infected mice.
  
  
  METHODS
  Mice were divided into four groups. Normal group, TNF treated group, P. y. nigeriensis infected group, and P. y. nigeriensis infected mice treated with TNF group (250 microg/kg body weight, i.p.).
  
  
  RESULTS
  TNF treatment of normal mice caused a highly significant decrease in hepatic superoxide dismutase (SOD) while changes in other oxidative stress and antioxidant defense indices were nonsignificant. On the other hand, TNF treatment of P. y. nigeriensis infected mice caused a highly significant increase in hepatic xanthine oxidase, lipid peroxidation and a significant decrease in hepatic SOD with respect to infected mice.
  
  
  CONCLUSIONS
  These results suggest that exogenous TNF acts synergistically with P. y. nigeriensis infection to generate oxidative stress in the host and also causes an impairment of antioxidant defense enzyme such as superoxide dismutase.
authors.affiliation: Department of Biochemistry, College of Science, King Saud University, Riyadh, Saudi Arabia.
authors.forename: N J
authors.initials: NJ
authors.lastname: Siddiqi
authors.forename: A S
authors.initials: AS
authors.lastname: Alhomida
authors.forename: B
authors.initials: B
authors.lastname: Sharma
authors.forename: V C
authors.initials: VC
authors.lastname: Pandey
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D008288:Malaria / Q000378:metabolism*; D051379:Mice; D018384:Oxidative Stress / Q000502:physiology*; D010967:Plasmodium yoelii; D011994:Recombinant Proteins / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase; D005980:Glutathione Reductase; D005978:Glutathione