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PubMed2000

Molecular characterization of a German variant of glucose-6-phosphate dehydrogenase deficiency (G6PD Aachen).

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-chromosome-linked hereditary disorder. Clinically, patients with G6PD deficiency often present with drug- or food-induced hemolytic crises or neonatal jaundice. G6PD is involved in the generation of NADPH and reduced glutathione. In contrast to American, Mediterranean, and African ancestries, only few variants are known from Middle and Northern Europe. We describe the molecular characterization of a distinct variant from the northwestern area of Germany, G6PD Aachen. The sequence of the G6PD gene from three afflicted males was found to be hemizygous at cDNA residue 1089 for a C-->G mutation with a predicted amino acid change of Asn363Lys. The 1089 C-->G point mutation is unique, but produces the identical amino acid change found in a Mexican variant of G6PD deficiency, G6PD Loma Linda. This G6PD-deficient variant is caused by a 1089 C-->A mutation. The 363-amino-acid replacement is located outside a known mutation cluster region between amino acid residues 380 and 450, but may disrupt or weaken dimer interactions of G6PD enzyme subunits.

Adult↗

PubMed1991

Mutation analysis of glucose-6-phosphate dehydrogenase (G6PD) variants in Costa Rica.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency has previously been reported among both the black and white populations of Costa Rica. All 28 G6PD A- samples were found to be of the common G6PD A-376G/202A type. A previously described mutation associated with nonspherocytic hemolytic anemia, G6PD Puerto Limón, was found to be due to a G----A transition at nucleotide (nt) 1192, causing a glu----lys substitution. Mutations in this region of the G6PD molecule seem invariably to be associated with chronic hemolytic anemia. G6PD Santamaria had been described previously in two unrelated white subjects. We found that both did, indeed, have the same mutations. In this variant the A----G substitution at nt 376 that is characteristic of G6PD A was present, but an A----T mutation at nt 542, apparently superimposed on the ancient G6PD A mutation, resulted in an asp----val substitution. Thus, the gain of a negative charge at amino acid 126 was counterbalanced by the loss of a charge at amino acid 181, giving rise to a variant with the G6PD A mutation but with normal electrophoretic mobility.

Black People↗

PubMed1993

Frequency of glucose-6-phosphate dehydrogenase (G6PD) mutations in Chinese, Filipinos, and Laotians from Hawaii.

In a Hawaii Hereditary Anemia Screening Project, 4,984 participants were tested for glucose-6-phosphate dehydrogenase (G6PD) deficiency by a filter paper blood spot fluorescence test. Abnormal samples and suspected heterozygotes were checked by quantitative G6PD assay (normal 4.5 to 14 units/g Hb). G6PD was deficient (< 1.5 units/g Hb) in 188 of 2,155 males; 7 other males had low activity (1.5 to 2.8 units/g Hb). The gene frequency, estimated from males after excluding referred and related cases, was 0.037 for Chinese, 0.134 for Filipinos, and 0.203 for Laotians. Among 2,829 females tested, family data showed 111 females were obliged to be at least heterozygous, regardless of G6PD activity, and 43 others had low G6PD activity. Most heterozygotes probably remained undetected by G6PD screening. In 28 females, activity was under 10%; in another 9 females, activity was < 1.5 units/g Hb. Since only 25 homozygotes would be predicted, this apparent excess of females with deficient activity could be due to unequal X-inactivation in some heterozygotes. DNA analysis by polymerase chain reaction amplification and special analytic procedures revealed 10 different missense mutations in 75 males. The nucleotide 835 A-->T and 1360 C-->T transitions were first detected in this Hawaiian Project; we found that the nucleotide 1360 mutation was the most common cause of G6PD deficiency in Filipinos. This is the first report of G6PD screening and analysis of molecular G6PD mutations in Filipino and Laotian populations.

Adult↗

PubMed2000

Enhanced oxidative stress and accelerated cellular senescence in glucose-6-phosphate dehydrogenase (G6PD)-deficient human fibroblasts.

Glucose-6-phosphate dehydrogenase (G6PD) is involved in the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) and the maintenance of the cellular redox balance. The biological effects of G6PD deficiency in nucleated cells were studied using G6PD-deficient human foreskin fibroblasts (HFF). In contrast to that of normal HFF, the doubling time of G6PD-deficient cells increased readily from population doubling level (PDL) 15 to 63. This was accompanied by a significant increase in the percentage of G(1) cells. The slow-down in growth preceded an early entry of these cells into a nondividing state reminiscent of cellular senescence. These cells exhibited a significant increase in level of senescence-associated beta-galactosidase (SA-beta-gal) staining. The importance of G6PD activity in cell growth was corroborated by the finding that ectopic expression of active G6PD in the deficient cells prevented their growth retardation and early onset of senescence. Mechanistically, the enhanced fluorescence in dichlorofluorescin (H(2)DCF)-stained G6PD-deficient cells suggests the possible involvement of reactive oxygen species in senescence. Taken together, our results show that G6PD deficiency predisposes human fibroblasts to retarded growth and accelerated cellular senescence. Moreover, G6PD-deficient HFF provides a useful model system for delineating the effects of redox alterations on cellular processes.

Cell Cycle↗

PubMed2003

Reduced prevalence of Plasmodium falciparum infection and of concomitant anaemia in pregnant women with heterozygous G6PD deficiency.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency confers protection against malaria in children, yet its role in malaria in pregnancy is unknown. In a cross-sectional study among 529 pregnant Ghanaian women, Plasmodium falciparum infection, anaemia and G6PD genotypes were assessed. Of these, 30.4% were heterozygous and 2.6% were homozygous for G6PD deficiency. The prevalence of P. falciparum infection decreased from 66% in G6PD-normal women to 58% in heterozygotes, and to 50% in individuals with homozygous G6PD deficiency (Chi2(trend) = 4.4, P = 0.04). Multivariate analysis revealed that in multigravid women but not in primigravidae, heterozygous G6PD deficiency was associated with a reduced risk of P. falciparum infection (Odds ratio (OR), 0.6; 95% confidence interval (95% CI), [0.4-0.9]). This protection against infection was limited to the third trimenon of pregnancy. In addition, heterozygous G6PD deficiency was associated with a reduced risk of anaemia among infected multigravidae (OR, 0.5 [0.3-1.0]). Pregnancy is a period of high vulnerability to malaria. The results of this study provide evidence for protection against malaria in pregnancy caused by heterozygous G6PD deficiency. This advantage, even if confined to multigravid women, may contribute to the selection of G6PD variants in malaria-endemic regions.

Adolescent↗

PubMed2006

Decreased glucose-6-phosphate-dehydrogenase (G6PD) activity and risk of senile cataract in Taiwan.

G6PD deficiency may render afflicted individuals more susceptible to certain degenerative diseases. To clarify the relationship between G6PD deficiency and cataract, blood G6PD activity was determined in patients with cataract in Taiwan. The cases and hospital-based controls were recruited from the medical outpatient department and from the physical checkup department at Chang Gung Memorial Hospital, respectively. A questionnaire survey was used to determine associations between cataracts and their risk factors. G6PD activity in fresh RBC was quantitatively measured and genomic DNA was extracted from lymphocyte nuclei. The mean blood G6PD activity among cataract patients (278.1 U/10[12] RBC) was similar to that of normals (288.0 U/10[12] RBC). No statistically significant difference in the distribution of G6PD activities as grouped by an increment of 100 U/[10, 12] RBC was observed between cataract patients and normal subjects. The predominant forms of G6PD gene mutation (cDNA 1376 G to T and 95 A to G) were both found in the patients with cataract. The adjusted odds ratio for cataract was 1.21 for every decrement of 100 U/10[12] RBC of G6PD activity in these subjects. These data indicate that G6PD activity is not a potential risk factor for senile cataract in Taiwan.

Aged↗

PubMed1988

The adaptation of Plasmodium falciparum to oxidative stress in G6PD deficient human erythrocytes.

It has recently been found that growth of P. falciparum in human G6PD deficient red cells is impaired in vitro; however, the inhibition is overcome after two or three growth cycles. There is evidence to suggest that the parasite can produce its own G6PD enzyme which may compensate for the lack of host enzyme and could account for the resumption of normal growth in G6PD deficient host cells. It is unclear whether the parasite enzyme can enable the host cell to resist oxidative stress as normal cells do. To answer this question, P. falciparum was grown in vitro in: (a) normal red cells, (b) G6PD deficient red cells for one growth cycle only, (c) G6PD deficient cells for a minimum of five cycles. All groups were then challenged with acetylphenylhydrazine (APH) which served as an oxidative stress. Both G6PD (A-) and Mediterranean deficient types were studied. The results show a two-fold increase in resistance to oxidative stress by parasites adapted to G6PD-Mediterranean deficient host cells as compared to unadapted ones, but the parasite-red cell system remains 4 times more sensitive to APH than normal infected cells. In parasitized G6PD (A-) red cells, evidence of adaptation could be seen in the growth curves, but no detectable increase in resistance to APH was found in adapted parasites. It is concluded that the role of the parasite G6PD is not likely to be mainly related to oxidative stress resistance and therefore other functions of this enzyme should be investigated.

Adaptation, Biological↗

PubMed1990

Common glucose-6-phosphate dehydrogenase (G6PD) variants from the Italian population: biochemical and molecular characterization.

By biochemical characterization of glucose-6-phosphate dehydrogenase (G6PD) from the red cells of seventeen subjects of the population of Matera (Southern Italy) we have identified six genetically determined common variants. Among these, G6PD Metaponto and G6PD A(-) Matera had been already fully characterized. We have now found that A(-) Matera is genetically heterogeneous since one of two subjects examined had the two mutations at codons 68 and 126 characteristic of a typical A(-) variant, while the other subject had only the codon 126 mutation. G6PD Pisticci and G6PD Tursi are two new variants whose molecular lesion is not yet known. G6PD Cagliari-like has biochemical characteristics reminiscent of G6PD Cagliari, isolated in Sardinia, and was found to have the same nucleotide substitution as G6PD Mediterranean. G6PD Montalbano is a new variant, with nearly normal properties, due to a G----A transition which causes an Arg----His amino acid replacement at position 285.

Alleles↗

PubMed2002

Molecular epidemiology and activity of erythrocyte G6PD variants in a homogeneous Nigerian population.

OBJECTIVE: To determine accurately the relative frequencies and enzyme activities of the polymorphic variants of G6PD in a homogeneous population in Nigeria. SETTING: Abanla village in the outskirt of Ibadan city and the University College Hospital, Ibadan Nigeria. SUBJECT: Seven hundred and twenty one subjects who belong to the Yoruba tribe of Southwestern Nigeria. METHOD: Two mls of blood was withdrawn from each subject. G6PD activity was quantified by spectrophotometry. DNA was extracted for genotyping of G6PD by PCR. RESULTS: G6PD deficiency was 23.9% and 4.6% in males and females respectively. The gene frequencies of the different G6PD variants (Gd) were in accordance with expected Hardy-Weinberg equilibrium. Only GdA-1 type was found in subjects with deficient variants. G6PD activity decreased significantly with age among non-deficient individuals. The range of enzyme activities was wide and overlapping among the different G6PD variants. CONCLUSION: G6PD deficiency was very high in the population. The gene frequencies were similar to previous findings. Molecular methods of typing G6PD allowed for direct and accurate genotyping of the enzyme in both males and females without having to combine several methods.

Adolescent↗

PubMed1999

Comparison of serum copper, magnesium, zinc and calcium levels between G6PD deficient and normal Chinese adults.

Minerals are important for normal hematopoiesis and may play a role in acute hemolytic anemia induced by G6PD deficiency. To compare serum magnesium, copper, zinc and calcium levels between G6PD deficiency and normal control adults, we investigated 69 G6PD deficient (28 male, 41 female) and 61 age- matched G6PD normal adults (26 male, 35 female). Serum magnesium, copper, zinc and calcium levels were determined by atomic absorbance spectrometry. Our results revealed that male adults with G6PD deficiency had significantly higher serum copper and magnesium levels than those of the control group (P < 0.01, < 0.05, respectively). In G6PD normal adults, serum copper levels were significantly lower in males than in females (P < 0.01). In the group of G6PD deficiency adults, serum copper levels in males (103.0 +/- 10.4 ug/dL) were significantly lower than those in females (139.0 +/- 34.3 ug/dL) (P < 0.01). Serum magnesium values and zinc values in males (2.42 +/- 0.38 mEq/L and 102.2 +/- 26.5 ug/dL) were significantly higher than those in females (2.07 +/- 0.20 mEq/L and 87.0 +/- 14.9 ug/dL) (P all < 0.01). Female adults with G6PD deficiency had significantly higher serum calcium levels and lower magnesium levels than those of the control group (P all < 0.01). The significantly higher levels of serum copper and magnesium in G6PD deficient male adults may play some role concerning red blood cells in resistance to plasmodium falciparum.

Adult↗

PubMed1999

Adequacy and pitfalls of G6PD deficiency counseling in Hong Kong.

Glucose-6-Phosphate-Dehydrogenase (G6PD) deficiency is common in Hong Kong with an incidence of 4.5% in male and 0.36% in female (Lo et al. 1996).The Neonatal Screening Unit of Clinical Genetic Service started its territory-wide neonatal screening program for G6PD deficiency and congenital hypothyroidism in 1984 (Lam et al, 1986). Because of insufficient manpower and resource, we have been giving health counseling on the phone to parents of G6PD deficient babies and then refer them to nearby maternal and child health centres for monitoring of jaundice. The disease, mode of inheritance, recurrence risk and the precaution against certain medicines (Chan 1996) and chemicals are explained. The purpose (Lam, 1994) is to reassure the parents that their G6PD deficient babies can be as normal as everyone and that they can have normal life. Nevertheless, it has not been established whether telephone counseling has any effect on the affected family in the form of psychological trauma (Marteau, 1989; Fyro, 1987; Li et al, 1996) or significant influence on the decision on future reproduction. This study tried to evaluate the service from the parents' point of view by 1) gathering information on parents' awareness and perception of G6PD deficiency, 2) determination of parents' attitude towards the telephone counseling, and 3) finding out the effect of G6PD deficiency on parents' decision on future reproduction. Over 300 parents were contacted by telephone, and were asked to respond to questions on a questionnaire . The telephone interview focused on parents' understanding of G6PD deficiency, their attitude towards this disease and the possible effect on future reproduction decision. Results showed that over 90% of cases that we had counseled attended the maternal and child health centres. Most of them accepted the presence of G6PD deficiency in their family which did not affect their decision on future pregnancy. Telephone counseling failed to establish a helping relationship with the parent as face to face counseling was more personal. The findings revealed that though telephone counseling had its shortcoming it served the target group effectively. Telephone counseling is still the method of choice for the G6PD deficiency counseling in this locality.

Adolescent↗

PubMed2005

[G6PD Gene Mutations in Shui people in Sandu of Guizhou].

UNLABELLED: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzymopathy. To date, about 126 mutations in the G6PD gene have been detected, among which 17 mutations were found in Chinese. The most common mutations are: 1376 G-->T and 1388 G-->A, both in exon 12; 95 A-->G in exon 2, which amounted to more than 50% of mutations representing various regions and ethnic groups in China. A large-scale screening and genotypic analysis was held in Shui people in Sandu of Guizhou. To investigate the incidence and the molecular basis of G6PD deficiency of Guizhou Shui people, NBT qualitative and G6PD/6PGD quantitative methods were used to detect G6PD deficiency in 1,090 Shui people from the general people belonging to Sandu of Guizhou. By means of mis-matched primers amplified the G6PD gene, the products were 234 bp, 280 bp and 345 bp in length, then restriction enzyme analysis was used to detect the most common Chinese G6PD mutations, 1376 G-->T, 1388 G-->A and 95 A-->G. The results showed that out of the 1,090 samples, 98 G6PD deficiency samples were found. The incidence of G6PD deficiency was 8.99%. 24 cases of 1376 G-->T, 12 cases of 1388 G-->A, 9 cases of 95 A-->G were detected. A sample with 1376 G-->T and 95 A-->G mutation was found in a girl. It was reported for the first time. IN CONCLUSION: 1376 G-->T, 1388 G-->A, 95 A-->G mutations are the common G6PD mutations in Shui people in Sandu of Guizhou. The results indicates that different national minorities of Chinese may originated from a common ancestor.

China↗

PubMed1992

A new mutation responsible for severe G6PD deficiency in two ethnic Chinese with different clinical presentations: determination by a direct PCR sequencing technique.

To test the hypothesis that clinical manifestation in G6PD deficiency correlates with a molecular lesion, we investigated the G6PD gene of two Chinese Americans both of whom had G6PD deficiency, but who manifested different clinical presentations. In this study, we have developed a direct PCR sequencing protocol to examine the human G6PD gene. By using optimized PCR conditions with internal primers, we were able to amplify a 4.2 kb DNA fragment (covering exon 3 through 13 of the G6PD gene) of consistently high quality. From this we were then able to generate high quality single-stranded DNA templates by asymmetric PCR for subsequent sequencing. We also overcame the crossband problem by using internal primers, high temperature reaction with Taq I DNA polymerase, and/or sequencing with gene 32 protein. We could consistently amplify exons 1 and 2 despite their high G/C content by substituting 75% of dGTP with deoxy-7-deaza-guanosine triphosphate. By using this novel approach, we have identified a new mutation at cDNA position 1376 from G to T, which causes substitution of Leu for Arg at amino acid position 459. This mutation has not been reported in other ethnic groups. It is the only genetic defect in the coding regions of the G6PD gene of these two G6PD deficient individuals. We speculate that in addition to a defect in the G6PD gene, other factors also play a role in the clinical manifestation of G6PD deficiency.

Base Sequence↗

PubMed1990

Origin and spread of the glucose-6-phosphate dehydrogenase variant (G6PD-Mediterranean) in the Middle East.

A common glucose-6-phosphate dehydrogenase (G6PD) variant characterized by severe enzyme deficiency and B-like electrophoretic mobility is called "G6PD-Mediterranean" because it is found in different populations around the Mediterranean Sea. Sequence analysis of Italian subjects has revealed that the molecular basis of G6PD-Mediterranean is a single C-T transition at nucleotide position 563, causing a serine phenylalanine replacement at amino acid position 188. Most G6PD-Mediterranean subjects also have a silent C-T transition (without amino acid replacement) at nucleotide position 1311. Twenty-one unrelated individuals from Saudi Arabia, Iraq, Iran, Jordan, Lebanon, and Israel with both severe G6PD deficiency and B-like electrophoretic mobility were tested for both mutations by using amplification followed by digestion with appropriate restriction enzymes. All but one had the 563 mutation, and, of these, all but one had the 1311 mutation. Another 24 unrelated Middle Eastern individuals with normal G6PD activity or not known to be G6PD deficient were similarly tested. Four had the silent mutation at position 1311 in the absence of the deficiency mutation at position 563. We conclude that (1) the large majority of Middle Eastern subjects with the G6PD-Mediterranean phenotype have the same mutation found in Italy, (2) the silent mutation is an independent polymorphism in the Middle East, with a frequency of about .13, and (3) the mutation leading to the G6PD-Mediterranean deficiency has probably arisen on a chromosome that already carried the silent mutation.

Base Sequence↗

PubMed1989

Two point mutations are responsible for G6PD polymorphism in Sardinia.

The human X-linked gene encoding glucose 6-phosphate dehydrogenase (G6PD) is highly polymorphic; more than 300 G6PD variants have been identified. G6PD deficiency in different geographical areas appears to have arisen through independent mutational events, but within the same population it may also be heterogeneous. One example is the island of Sardinia, where careful clinical and biochemical studies have identified four different G6PD variants. We cloned and sequenced the four G6PD variants from Sardinia and found that only two mutations are responsible for G6PD deficiency in this area: one mutation is the cause of the G6PD Seattle-like phenotype, a milder form of G6PD deficiency; the other mutation is responsible for all forms of very severe G6PD deficiency in Sardinia and, possibly, in the Mediterranean.

Cloning, Molecular↗

PubMed1986

Excess release of ferriheme in G6PD-deficient erythrocytes: possible cause of hemolysis and resistance to malaria.

Hemoglobin in glucose-6-phosphate dehydrogenase (G6PD)-deficient erythrocytes is abnormally vulnerable to oxidative denaturation, which may release ferriheme, a known cytolytic agent. We found 13.3 nmol of ferriheme in G6PD-deficient erythrocyte membranes (per gram of total erythrocyte hemoglobin) using a spectrophotometric assay, as compared to 9.8 in normal membranes (P less than .05). After incubation of erythrocytes with 250 mumol/L menadione, an oxidant drug, the values increased by 37.4 nmol in G6PD-deficient membranes and by 26 in normal membranes (P less than .005), indicating increased hemoglobin denaturation. To verify that hemoglobin denaturation in G6PD-deficient erythrocytes releases ferriheme in a form available to interact with other ligands, [14C]-chloroquine binding to intact erythrocytes was measured. With an initial concentration of 5 mumol/L chloroquine in a medium containing no menadione, an excess of 14.8 nmol of chloroquine was bound in G6PD-deficient erythrocytes (per gram of hemoglobin) as compared to normal erythrocytes (P less than .005). In the presence of 250 mumol/L menadione, chloroquine binding increased by 17.9 nmol in G6PD-deficient and by 7.2 in normal erythrocytes (P less than .005). These results indicate that ferriheme becomes available to interact with endogenous ligands and, thus, to mediate menadione-induced hemolysis in patients with G6PD deficiency. Furthermore, the increase in ferriheme may mediate the selective toxicity of menadione for Plasmodium falciparum parasites growing in G6PD-deficient erythrocytes. Ferriheme release in response to the intraerythrocytic oxidant stress introduced by malaria parasites also may account for the resistance to malaria afforded by G6PD deficiency. This is a US government work. There are no restrictions on its use.

Chloroquine↗

PubMed1997

[The role of NADPH in the development of neonatal jaundice with G6PD deficiency].

OBJECTIVE: To investigate the role of NADPH in the development of neonatal jaundice with G6PD deficiency. METHODS: The enzyme activities of G6PD, catalse (Cat) and glutathione peroxidase (GSH-px) were measured by quantitative determination of enzyme activity. The level of MDA was analyzed with alpha-thiobarbituric acid and the level of NADPH was determined with modified Nisselbaum JS's. Comparisons of these markers between G6PD normal and deficient erythrocytes were made before and during the incubation of the erythrocytes with H2O2. RESULTS: The level of MDA, which was 36 +/- 8n-mol.L-1.gHb-1, was increased and that of NADPH, which was 1792 +/- 106mumol.L-1.gHb-1, was decreased in jaundiced neonates with G6PD deficiency compared with those with normal G6PD activity. When the cells were incubated with H2O2, the level of NADPH and the activities of Cat and GSHpx in erythrocytes with normal G6PD activity increased at first, and then turned to decrease as the incubation lasted longer than 30 minutes. But in G6PD-deficient erythrocytes all these markers decreased continuously as the cells were incubated with H2O2. CONCLUSIONS: The diminished capability of generation of NADPH in G6PD-deficient erythrocytes may contribute directly to the more extensive peroxidation of the cells. The defect capacity of generation of NADPH, which resulted in the weakened capability of antiperoxidation and finally the lysis of erythrocytes, was one of the important mechanisms in the development of jaundice in G6PD-deficient neonates.

Glucosephosphate Dehydrogenase Deficiency↗

PubMed2003

Two cases of glucose-6-phosphate dehydrogenase-deficient Nepalese belonging to the G6PD Mediterranean-type, not India-Pakistan sub-type but Mediterranean-Middle East sub-type.

In Nepal, we tested 300 males for glucose-6-phosphate dehydrogenase (G6PD) activity. Two subjects were G6PD deficient (0.67%). Compared with normal controls, G6PD activity was 12% and 26%, respectively. The hemoglobin concentration of these two subjects was normal. We extracted genomic DNA from whole blood and read all sequences of G6PD. Both subjects had the same replacement of 563C>T, which was classified as G6PD Mediterranean. The amino acid might change from Ser to Phe at codon 188. These subjects also had a replacement of 1311C>T, which caused no replacement of an amino acid. A similar replacement pattern of G6PD Mediterranean is described from persons living in Mediterranean countries and Middle East countries. However, G6PD Mediterranean found in India and Pakistan has no replacement at nucleotide 1311. Thus, these two subjects in Kathmandu, Nepal, would be closer to people in Middle East countries than people in India. This is the first study of molecular analysis for G6PD deficiency in Nepal.

Adolescent↗