Malaria Protection In Glucose-6-Phosphate Dehydrogenase Deficient Individuals In Bamenda Population Of Cameroon

The high frequency of glucose-6-phosphate dehydrogenase (G6PD) deficiency gene in malaria endemic regions is believed to be due to the enzyme deficiency advantage against fatal malaria. However, the mechanism of this protection is not well understood and therefore was investigated by comparing differences in plasmodial parasitaemia, full blood count profile and the severity of clinical malarial symptoms of G6PD deficient and G6PD non–deficient cohort groups in the population. Our results showed that 10.4% (63/606) of those tested carried the G6PD deficiency gene. G6PD deficient heterozygous females and hemizygous males manifested significantly reduced (

Influence of sickle heterozygous status and glucose-6-phosphate dehydrogenase deficiency on the clinico-haematolgoical profile of Plasmodium falciparum-infected children

Sickle haemoglobin (HbS) and glucose–6–phosphate dehydrogenase (G6PD) enzyme deficiency genes are known to offer reliable protection against falciparum malaria in malaria endemic areas of the world. However, the mechanism of protection is not yet completely understood. In this study, we investigated the contribution of HbS and G6PD enzyme deficiency status in ameliorating the severity of malaria attack by comparing the clinical symptoms, parasitaemia andhaematological profiles of Plasmodium falciparum–infected volunteer children. The selected group of children, G6PD deficient sickle heterozygotes (HbAS) (n = 5), G6PD non–deficient HbAS (n = 30), G6PD deficient dominant homozygotes (HbAA) (n = 10) and G6PD non–deficient HbAA (n = 30) were monitored for a period of one year with a view to elucidating further the involvement of HbS and G6PD enzyme deficiency in the protection of children against plasmodial infection. Results revealed greater severity (indicated by malarial anaemia), higher incidence of atypical thrombocytopenia, high white blood cell (WBC) counts and significantly higher (P < 0.05) parasite density and percentage parasitaemia in G6PD non–deficient HbAA subjects compared to G6PD non–deficient HbAS, G6PD deficient HbAS subject and G6PD deficient HbAA. Less severe clinical malarial symptoms were also observed more in G6PD deficient HbAS when compared to G6PD non-deficient HbAA subjects during malariaattack. These results seem to indicate that inheriting both genetic defects reduces the profligacy of malaria parasite and hence, ameliorate the severity of acute falciparum malaria. Consequently, selective advantage against fatal falciparum malaria seems to be conferred since malarial anaemia, parasitaemia and severe malarial symptoms were significantly reduced

Free radical scavenging activity and phenolic contents of Anthocleista djalonensis (Loganiaceae) leaf extract

Anthocleista djalonensis extract is widely used in Nigerian folk medicine to treat conditions whose pathogenesis implicate oxidative stress, such as diabetes and hepatitis. However, little is known of the mechanism underlying these activities. In this study, the free radical scavenging potential of a methanol extract of A. djalonensis leaves was assessed by measuring its capability for scavenging 2,2-diphenyl-1-picrylhydrazyl(DPPH.) radical, superoxide anion radical (O2.–), hydroxyl radical (.OH), nitric oxide radicals (NO.), as well as its ability to inhibit lipid peroxidation, using appropriate assay systems compared to natural and syntheticantioxidants. Total phenolic, flavonoid and flavonol contents were determined by spectrophotometric methods. This extract showed a very potent DPPH. and O2 .– anion radical scavenging activities (IC50 = 8.69 ± 0.95 ìg/ml and 5.32 ± 1.05 ìg/ml respectively) and also significantly inhibited the accumulation of nitrite in vitro. The .OH radical and non-enzymatic lipid peroxidation inhibitory potentials of the extract were significantly higher (

Association of glucose-6-phosphate dehydrogenase deficiency and malaria: a systematic review and meta-analysis

Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency overlaps with malaria endemicity although it predisposes carriers to hemolysis. This fact supports the protection hypothesis against malaria. The aim of this systematic review is to assess the presence and the extent of protective association between G6PD deficiency and malaria. Thirteen databases were searched for papers reporting any G6PD alteration in malaria patients. Twenty-eight of the included 30 studies were eligible for the meta-analysis. Results showed absence of negative association between G6PD deficiency and uncomplicated falciparum malaria (odds ratio (OR), 0.77; 95% confidence interval (CI), 0.59-1.02; p = 0.07). However, this negative association happened in Africa (OR, 0.59; 95% CI, 0.40-0.86; p = 0.007) but not in Asia (OR, 1.24; 95% CI, 0.96-1.61; p = 0.10), and in the heterozygotes (OR, 0.70; 95% CI, 0.57-0.87; p = 0.001) but not the homo/hemizygous (OR, 0.70; 95% CI, 0.46-1.07; p = 0.10). There was no association between G6PD deficiency and total severe malaria (OR, 0.82; 95% CI, 0.61-1.11; p = 0.20). Similarly, there was no association with other malaria species. G6PD deficiency can potentially protect against uncomplicated malaria in African countries, but not severe malaria. Interestingly, this protection was mainly in heterozygous, being x-linked thus related to gender