The present study was aimed at determining and comparing the effects of Artecxin (ART), P - Alaxin (P-ALA), Lonart (LON) and Chloroquine (CQ) on oxidative stress parameters and mitochondrial membrane composition in the course of malaria infection. Six groups of five mice each categorized as healthy control (non-parasitized non-treated group), parasitized-non-treated (PnT), parasitized-chloroquine-treated (positive control), parasitized-Artecxin, -Lonart and -P-Alaxin-treated groups were used for the study. Hepatic antioxidant status was assessed with levels of malondialdehyde (MDA) and reduced glutathione (GSH) as well as activity of superoxide dismutase (SOD) and catalase (CAT) in the post mitochondrial and mitochondrial fractions. Mitochondrial membrane integrity was also evaluated with activity of succinate dehydrogenase and levels of phospholipids, cholesterol and proteins in the liver mitochondria. Results revealed that treatment of parasitized mice with the antimalarial drugs significantly (p<0.05) decreased hepatic malondialdehyde (MDA) and mitochondrial membrane phospholipids compared to parasitized untreated group. On the other hand, significantly (p<0.05) elevated succinate dehydrogenase (SDH) activity, mitochondrial membrane cholesterol level, GSH concentration, catalase (CAT) and superoxide dismutase (SOD) activity in the post mitochondrial fraction were obtained. Thus, antimalarial drugs distort mitochondrial membrane integrity and electron transfer but reduce the malaria-induced oxidative stress on the host.
Malaria is an important health and development challenge in Africa, Animal models most particularly mice, have long been employed to study malaria pathogenesis. This paper describes clinical manifestations due to Plasmodium berghei ANKA infection in juvenile mice as a model for understanding the complications of congenital malaria in neonates. Forty-five juvenile mice (5-7 days old) were acquired from University College Hospital, Ibadan and injected with 2×107 (0.2 ml) Plasmodium berghei ANKA parasitized red blood cells (PRBCs). The mice were then transported to the study site, kept in well-ventilated cages and fed daily with a balanced ration. Post-P. berghei infection, the mice were monitored daily for mortality. Clinical manifestations of experimental cerebral malaria (ECM) were assessed and confirmed if at least ruffled fur, hunching, wobbly gait, limb paralysis, convulsions, or coma was observed. Each sign was given a score of 1. Animals with scores ≥4 were considered to have severe ECM. In the experiment, 20 (44%) mice were lost due to natural cause (i.e. stress) at day 2. Between day 4 and 9, 25 (56%) of the study mice presented clinical signs of ECM. This included: ruffled fur – 25 (100%), hunching - 21 (84%), wobbly gait - 17 (68%), limb paralysis - 20 (80%), convulsions - 25 (100%). Survival rate and severity of ECM in the mice differs, 22 (88.0%) had severe ECM and 3 (12.0%) had mild ECM. This study has shown that parasite establishment and malaria complications can manifest as early as 4 days’ post P. berghei infection in 5-7 days old mice.
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