title: Status of hepatic oxidative stress and antioxidant defense systems during chloroquine treatment of Plasmodium yoelii 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 have been implicated in the pathogenesis of malaria.
  
  
  OBJECTIVE
  Study the effect of the chloroquine treatment on hepatic oxidative stress and antioxidant defense indices in multiple drug resistant (MDR) P. y. nigeriensis infected mice.
  
  
  METHODS
  Mice were divided into four groups. Normal group, chloroquine treated normal group, P. y. nigeriensis infected group, and P. y. nigeriensis infected mice treated with chloroquine group (10 mg/kg body weight, i.p.).
  
  
  RESULTS
  P. y. nigeriensis infection resulted in a significant decrease in the hepatic protein levels and caused a significant increase in the hepatic oxidative stress indices such as xanthine oxidase and lipid peroxidation and also an increase in the antioxidant defense indices viz, reduced glutathione (GSH), and glutathione reductase, but a significant decrease in superoxide dismutase (SOD) and catalase. The chloroquine treatment of P. y. nigeriensis (MDR strain) infected mice did not completely cure blood parasitemia, but resulted in a decrease of blood parasitemia. This was accompanied by decrease in hepatic oxidative stress indices and an associated change in the antioxidant defense indices towards normalization.
  
  
  CONCLUSIONS
  Chloroquine therapy alone is not sufficient to treat the malaria infection caused by multiple drug resistant strain of P. y. nigeriensis. Therefore, there is a need to develop newer antimalarials which could act alone or in combination with traditional antimalarials to be effective against drug resistant malarial parasites.
authors.affiliation: Department of Biochemistry, College of Science, King Saud University, Riyadh, Saudi Arabia. nikhat@ksu.edu.sa
authors.forename: N J
authors.initials: NJ
authors.lastname: Siddiqi
authors.forename: A S
authors.initials: AS
authors.lastname: Alhomida
mesh_terms: D000818:Animals; D000962:Antimalarials / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D002738:Chloroquine / Q000494:pharmacology*; D018432:Drug Resistance, Multiple; D005978:Glutathione / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000201:enzymology* / Q000469:parasitology; D008288:Malaria / Q000188:drug therapy* / Q000378:metabolism; D051379:Mice; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress / Q000502:physiology*; D010967:Plasmodium yoelii; D013482:Superoxide Dismutase / Q000378:metabolism; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D000962:Antimalarials; D002738:Chloroquine; D002374:Catalase; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase; D005980:Glutathione Reductase; D005978:Glutathione