Oxidant status of children infected with plasmodium falciparum malaria in Katsina metropolis, Northwestern Nigeria

Background: Malaria is a global menace caused by the transfer of a plasmodium parasite to a host by an infected anopheles mosquito. Upon infection; the overwhelmed host releases free radicals which have the capacity to induce oxidative damage by lipid peroxidation. This study was undertaken to assess the effect of malaria caused by Plasmodium falciparum on some antioxidant markers and lipid peroxidation levels in children attending hospitals in Katsina State; Nigeria. Materials and Methods: Blood samples were collected from untreated subjects upon confirmation of Plasmodium falciparum parasitaemia using the Giemsa stain technique. One hundred and sixty (160) consenting individuals (80 infected patients and 80 uninfected subjects) comprising of both sexes were randomly selected. The levels of antioxidant markers and malondialdehyde (MDA) - a lipid peroxidation marker were determined. Descriptive analysis was employed using SPSS version 16.0 and significance between groups was ascertained using students' T-test. Results: P. falciparum malarial infection significantly (p 0.05) reduced the antioxidant markers [vitamins A; C; et E; and reduced glutathione (GSH)] by 65.4%; 29.7%; 48.1%; 40.4% respectively in males and by 54.2%; 36.6%; 55.7% ; 36.6% in females when compared with values obtained from uninfected; healthy children. Conversely; lipid peroxidation levels were significantly (p 0.05) higher in children with parasitaemia than in nonparasitaemic controls. Males showed greater than 200% increase; while it increased by 138% in females. Conclusion: Our findings indicate a reciprocal relationship; where high levels of lipid peroxidation correspond to low levels of antioxidants; which may be due to over utilization of the antioxidants in order to counteract the effect of free radicals. This may be responsible for oxidative stress and consequently; tissue damage associated with pathology of malaria in Nigerian children

Regional accumulation of aluminium in the rat brain is affected by dietary vitamin E.

The regional accumulation of aluminium in the brain of male albino Wistar rats was investigated following 4 weeks of administration by intraperitoneal injection of aluminium lactate (10mg aluminium/kg body weight). The consequences of concomitant dietary vitamin E (5, 15, or 20 mg vitamin E/g of food) were also studied. Rat brains were dissected into functional regions, for the measurement of aluminium and markers of oxidative stress. Plasma aluminium levels were increased in all groups of animals receiving aluminium lactate (p < 0.01), and these levels were significantly reduced in rats receiving concomitant vitamin E (p < 0.05). In the group of rats receiving aluminium alone, levels of brain tissue aluminium were increased in all regions of brain examined (p< 0.01). Brain tissue aluminium levels were reduced by concomitant dietary vitamin E. Catalase and reduced glutathione levels were both reduced in several regions of brain in animals treated with aluminium (p < 0.05). Aluminium treatment was not associated with a significant increase in reactive oxygen species (ROS) generation (p > 0.05), although ROS production was attenuated by dietary vitamin E (p < 0.05) in some regions.

Aluminium administration is associated with enhanced hepatic oxidant stress that may be offset by dietary vitamin E in the rat.

It has been proposed that aluminium toxicity may be mediated, at least in part, by free radical generation. We have investigated the effects of aluminium lactate administration on indices of hepatic oxidant stress, and the consequences of concomitant dietary vitamin E, in male albino Wistar rats. Aluminium lactate was administered for 4 weeks, by ip injection at 10 mg aluminium/kg body weight. Groups of animals received a chow diet containing 0, 5, 15, or 20 mg vitamin E/g of food. A control group of rats received a normal chow diet, without being injected with aluminium. The rats were killed after 4 weeks, and blood and liver tissue removed for the measurement of aluminium and markers of oxidative stress. Plasma and liver aluminium levels were increased in all groups of animals receiving aluminium lactate (P < 0.01), although these levels were significantly reduced in rats receiving concomitant vitamin E (P < 0.05). Aluminium treatment was associated with significantly increased levels of hepatic reactive oxygen species (ROS) (P < 0.01) that were attenuated by concomitant vitamin E (P < 0.05). Hepatic catalase and reduced glutathione levels were both reduced in animals treated with aluminium (P < 0.05).

Hypoglycemic and hypolipidemic effects of aqueous extract of Arachis hypogaea in normal and alloxan-induced diabetic rats.

The hypoglycemic and hypolipidemic effect of aqueous extract of Arachis hypogaea was investigated in normal and alloxan-induced diabetic rats. The extract caused a significant (P < 0.05) decrease of fasting blood glucose of both normal and alloxan-induced diabetic rats from 102.60 +/- 1.65 mg/dl to 88.79 +/- 0.94 mg/dl for normal and 189.0 +/- 30.79 mg/dl to 107.55 +/- 1.54 mg/dl for alloxan-induced diabetic rats. The extract also caused a significant (P < 0.05) decrease in serum triglyceride, total cholesterol, HDL-cholesterol and LDL-cholesterol in both normal and alloxan-induced diabetic rats.