Abdulkareem, A.OBabamale, O.AAishat, L.AAjayi, O.CGloria, S.KOlatunji, L.AUgbomoiko, U.S2023-04-032023-04-032020-10-11https://uilspace.unilorin.edu.ng/handle/20.500.12484/8973Malaria is a global health problem with severe morbidity and mortality in Sub-Saharan Africa. Resistance of Plasmodium spp to the current anti-malaria drugs necessitates further search for novel effective drugs. This study, therefore, investigated the effect of sodium acetate on glucose-6-phosphate dehydrogenase in Plasmodium berghei-infected mice. Thirty male Albino mice were randomly distributed into 6 groups, A–F. Animals in Groups B–F were inoculated with P. berghei, intraperi toneally. Subsequently, Group C mice were treated with 20 mg/kg chloroquine, while groups D, E and F received 25, 50 and 100 mg/kg sodium acetate, respectively. All treat ments were administered orally for 4 days. At the end of the experiment, animals were sacrificed by cervical dislo cation and blood was collected via cardiac puncture for the analyses of serum glucose-6-phosphate dehydroge nase (G6PD), uric acid and lipid profile. Our results sho wed that Sodium acetate (50 and 100 mg/kg) significantly reduced (p\ 0.05) parasitaemia (67.11% and 77.62%, respectively) than chloroquine (61.73%). Besides, body weight and serum G6PD activity in P. berghei infection were improved. Similarly, sodium acetate reduced elevated serum uric acid. Effects of sodium acetate and chloroquine on biochemical parameters were comparable (p [0.05) but atherogenic lipid ratios were not affected by sodium acetate. These data put together suggested that activity of sodium acetate may be harnessed for development of novel anti-malaria drugs. However, more studies are required to delineate its mechanisms of action.Sodium acetatePlasmodium bergheiUric acidLipid profileG6PDArticle