Influence of chloroquine treatment and Plasmodium falciparum malaria infection on some enzymatic and non-enzymatic antioxidant defense indices in humans.
BACKGROUND
It is known that malaria infection is accompanied by increased production of reactive oxygen species (ROS) and that malaria parasites are sensitive to oxidative damage. This has been proved by the efficacy of some antimalarial drugs that are known to act via generation of ROS when administered clinically or experimentally.


OBJECTIVE
There is lack of information on the effect of chloroquine on the antioxidant defense systems of normal and malaria infected humans. Since chloroquine has remained the mainstay of therapeutic regimen in malaria endemic zones, the present investigation was therefore undertaken to study the status of blood antioxidant defense mechanism, and oxidative stress following chloroquine treatment in normal and plasmodium infected humans.


METHODS
Ten healthy persons (5 males and 5 females) with the same age range (18-35 years) were taken as control group. Ten other individuals were treated with 25 mg/kg body with chloroquine over three days. Ten patients with malaria, not under antimalarial therapy were taken as another group, while another set of 10 patients with malaria were treated with 25 mg/kg body weight over three days.


RESULTS
The activity of superoxide dismutase was increased by 23% in individuals treated with chloroquine compared to controls while the activity of the enzyme decreased by 26% in malaria patients and by 43% in malaria patients treated with chloroquine. In all the treatment groups, the activities of catalase and glutathione peroxidase were lowered (P < 0.001). Similarly the levels of vitamins A, C, and beta-carotene were decreased in the treatment groups while plasma ceruloplasmin was increased in the groups. Glutathione and cholesterol levels were decreased while malondialdehyde level was increased significantly.


CONCLUSIONS
Chloroquine treatment mediated oxidative stress in the host and this effect was exacerbated in Plasmodium falciparum infected patients administered with the drug.
Farombi
E Olatunde
EO
Department of Biochemistry, Drug Metabolism and Toxicology, Research Laboratories, College of Medicine, University of Ibadan, Nigeria. olatunde_farombi@hotmail.com
Shyntum
Yvonne Y
YY
Emerole
Godwin O
GO
D000293:Adolescent; D000328:Adult; D000818:Animals; D000962:Antimalarials / Q000009:adverse effects* / Q000627:therapeutic use; D002374:Catalase / Q000378:metabolism; D002570:Ceruloplasmin / Q000378:metabolism; D002738:Chloroquine / Q000009:adverse effects* / Q000627:therapeutic use; D002784:Cholesterol / Q000378:metabolism; D004912:Erythrocytes / Q000187:drug effects* / Q000201:enzymology; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects; D016778:Malaria, Falciparum / Q000097:blood / Q000201:enzymology*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D010963:Plasmodium falciparum / Q000302:isolation & purification*; D013482:Superoxide Dismutase / Q000378:metabolism; D014815:Vitamins / Q000097:blood
D000962:Antimalarials; D014815:Vitamins; D002738:Chloroquine; D002784:Cholesterol; D002374:Catalase; D013482:Superoxide Dismutase; D002570:Ceruloplasmin