Effect of poly ICLC treatment on hepatic oxidative stress and antioxidant defense indices in Plasmodium yoelii nigeriensis infected mice.
BACKGROUND
Plasmodium yoelii nigeriensis (P. y. nigeriensis) produces lethal malaria infection in Swiss albino mice. Reactive oxygen species (ROS) are important mediators of tissue injury during malaria infection.


OBJECTIVE
To study the status of hepatic oxidative stress and antioxidant defense indices during Plasmodium yoelii nigeriensis (P. y. nigeriensis) infection and poly ICLC treatment of normal and P. y. nigeriensis infected Swiss albino mice.


METHODS
Mice were divided into four groups viz., 1. Normal mice, 2. Normal mice treated with poly ICLC (5 mg/kg body weight, i.p.), 3. P. y. nigeriensis infected mice and 4. P. y. nigeriensis infected mice treated with poly ICLC (5 mg/kg body weight, i.p.).


RESULTS
P. y. nigeriensis infection caused a significant increase in hepatic oxidative stress indices viz., xanthine oxidase and lipid peroxidation. This was accompanied by a significant increase in antioxidant defense indices viz., reduced glutathione (GSH), glutathione reductase while superoxide dismutase and catalase showed a significant decrease with respect to normal mice. Poly ICLC treatment of P. y. nigeriensis infected mice did not cure blood parasitemia. However, poly ICLC treatment of normal and P. y. nigeriensis resulted in an increased generation of hepatic oxidative stress and an associated increase in the antioxidant defense indices.


CONCLUSIONS
poly ICLC 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 antimalarias which can act alone or in combination with traditional antimalarials to be effective against drug resistant malarial parasite.
Siddiqi
N J
NJ
Department of Biochemistry, King Saud University, PO Box 2455, Riyadh 11451, Saudi Arabia. nikhat@ksu.edu.sa
Alhomida
A S
AS
Maheshwari
R K
RK
Pandey
V C
VC
D000818:Animals; D002266:Carboxymethylcellulose Sodium / Q000031:analogs & derivatives / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007369:Interferon Inducers / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000201:enzymology / Q000469:parasitology / Q000473:pathology; D008288:Malaria / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D051379:Mice; D009929:Organ Size; D018384:Oxidative Stress / Q000187:drug effects*; D010967:Plasmodium yoelii; D011070:Poly I-C / Q000494:pharmacology*; D011107:Polylysine / Q000031:analogs & derivatives / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism; D014969:Xanthine Oxidase / Q000378:metabolism
D002266:Carboxymethylcellulose Sodium; D002374:Catalase; D005978:Glutathione; D005980:Glutathione Reductase; D007369:Interferon Inducers; D011070:Poly I-C; D011107:Polylysine; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase; C019531:poly ICLC