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Results for “GLUCOSEPHOSPHATE DEHYDROGENASE”

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At least 991 records · Page 55Linked to original sources
PubMed1980

[Patterns in the distribution of GPD- alleles in Azerbaijan. I. Incidence and polymorphism of glucose-6-phosphate dehydrogenase deficiency in the Shekii region of the Azerbaijan SSR].

Through examination of G6PD deficiency among 939 pupils of Shekii district of Azerbaijan 52 hemi-, 10 homo- and 58 heterozygous carriers of defect were found. Relatives of probands--inhabitants of 3 settlements in the Shekii district-- were examined on G6PD deficiency too. Average hemizygote frequency is 11.11%, heterozygotes frequency is 12.9%. The cases of disaccordance between phenotype and genotype in female carriers of Gd- are analysed using pedigree data.

Alleles↗
PubMed1988

Characterization of a new glucose-6-phosphate dehydrogenase variant: G6PD Central City.

Glucose-6-phosphate-dehydrogenase deficiency is the most common disease-producing enzyme deficiency in man. This paper describes a new glucose-6-phosphate-dehydrogenase variant discovered during the evaluation of an episode of acute hemolytic anemia in a 62-year-old black male, which was temporally related to the ingestion of Tolbutamide. The hemolysis resolved within 10 days despite continuation of Tolbutamide. The erythrocyte glucose-6-phosphate-dehydrogenase activity was significantly decreased, and its electrophoretic mobility was indistinguishable from wild type enzyme, though faster on starch gel with tris, borate, and phosphate buffers. The enzyme had a biphasic pH optimum reduced Km for G-6-P and NADP, decreased utilization of deamino-NADP, and reduced Ki for NADPH. Because the kinetic properties of this enzyme were unique, we have designated it as G6PD Central City.

Alabama↗
PubMed1992

G-6PD deficiency in malaria endemic areas of Udaipur District in Rajasthan.

Nine thousand four hundred thirty three pyrexial cases were screened for the evidence of Malaria and Glucose-6-phosphate dehydrogenase deficiency among the rural tribal population of seven primary health centres in the malarial endemic areas of Udaipur District in Southern Rajasthan. One thousand four hundred five (P. Falciparum 831 and P. Vivax 574) cases were positive for malaria and 170 for G-6PD deficiency. Incidence of G-6PD deficiency in malaria, when compared to the non-malarial cases revealed statistically insignificant alterations (X2 is calculated to 0.1299 which for 1 degree of freedom gives P > 0.05).

Glucosephosphate Dehydrogenase↗
PubMed1984

[Possible regulatory importance of cellular sulfhydryl groups and reduction metabolic pathways for the activation of human blood platelets].

The activation of the blood platelets is the prerequisite for their participation in physiological and pathological intravasal processes. An aimed influence on the distinct functions of the blood platelets presumes an exact knowledge about course and regulation of the activation of the platelets. Investigations on glucose-6-phosphate-dehydrogenase-deficient platelets and on the effect of glutathione-oxidizing substances on normal platelets showed references to a regulatory significance of the cellular thiol/disulphide state in the process of activation. In this case particularly the arachidonic acid balance and the SH/SS-state of platelet proteins seem to be in close connection with reductive ways of metabolism.

Arachidonic Acids↗
PubMed1966

Glucose-6-phosphate dehydrogenase activity in erythrocytes of experimental animals.

Guinea-pigs, rats, dogs, rabbits, monkeys, sheep, and goats were screened for G-6PD activity in erythrocytes by the methaemoglobin reduction test, the brilliant cresyl blue decolorization test, and the spectrophotometric determination of the NADPH generation rate. Guinea-pigs, rats, dogs, rabbits, and monkeys were found to have normal G-6PD activity in erythrocytes, whereas sheep and goats were profoundly deficient in this enzyme. There was no evidence of any haemolytic anaemia in sheep and goats at the time of study. The relative sensitivity of these tests is discussed.

Animals↗
PubMed1984

G6PD Cagliari: a new low activity glucose 6-phosphate dehydrogenase variant characterized by enhanced intracellular lability.

A new variant of human erythrocyte glucose 6-phosphate dehydrogenase (G6PD), designated G6PD Cagliari, has been characterized. It is associated with severe enzyme deficiency and can be placed in Class 2 of the usual tabulation of G6PD variants. The specific activity of this variant is near normal, while its decay within the circulating erythrocytes is very rapid compared with normals. Genetic analysis of the family of the propositus indicated that the two available females are heterozygotes characterized by extremely unbalanced mosaic phenotypes.

Adolescent↗
PubMed1985

A new glucose-6-phosphate dehydrogenase variant, Gd(-) Tepic, characterized by moderate enzyme deficiency and mild episodes of hemolytic anemia.

A 16-year-old Mexican male of Japanese ancestry was found to have a new glucose-6-phosphate dehydrogenase (G-6-PD) deficient variant, named Gd(-) Tepic after the birthplace of the maternal grandmother. A younger brother was also affected and the two sisters were heterozygous. The mother, an obligatory heterozygote, did not show the abnormal variant and the possible explanation of this phenomenon is discussed. From the clinical standpoint, the propositus has had three mild hemolytic episodes while his siblings are so far asymptomatic.

Adolescent↗
PubMed2006

The role of the G6PD AEth376G/968C allele in glucose-6-phosphate dehydrogenase deficiency in the seerer population of Senegal.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is common in tropical Sub-Saharan countries. The allele most frequently associated with G6PD deficiency in this a region is G6PD 376G/202A. Here, we show that, the prevalence of G6PD deficiency is 12% in the Sereer ethnic group from Senegal ant that the 376G/968C genotype is predominant; the frequency of the 376G/202A genotype is very low in this ethnic group.

Alleles↗
PubMed1993

Study of glucose-6-phosphate dehydrogenase (G6PD) in the Kissan tribals of Orissa and the Kannikar tribals of Kerala, India.

G6PD deficiency has been studied in two tribal populations: Kissan tribals of Orissa and Kannikar tribals of Nedumungad Taluk, Trivandrum, Kerala. The percentage frequencies of G6PD deficiency are 14.13% and 5.5%, respectively. The two areas have a different pattern with respect to malarial infection. The Orissa one is an endemic malaria zone, while the Kerala one is less malarious. This is very well reflected by the frequency distribution of G6PD deficiency.

Cross-Cultural Comparison↗
PubMed1991

Clinical utility of fractionating erythrocytes into "Percoll" density gradients.

Two rapid methods for fractionating the RBC into five or nine layers of increasing density are reported. These procedures have been used to monitor the decline of glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD) activity during the process of red cell aging in normal subjects and in beta-thal carriers, to study transfused patients with G6PD and pyruvate kinase (PK) deficiency and to test the effects of inositol hexaphosphate (IHP) encapsulation on RBC subpopulations.

Adult↗
PubMed1982

Separate detection of glucose-6-phosphate dehydrogenase from 6-phosphogluconate dehydrogenase by DEAE-paper chromatography.

Red blood cell lysates were applied to DEAE cellulose paper for detection of glucose-6-phosphate dehydrogenase. Glucose-6-phosphate dehydrogenase (G-6-PD) was separated from 6-phosphogluconate dehydrogenase (6-PGD) by DEAE-cellulose paper-chromatography and their activities were detected on the chromatogram by applying the reaction mixture. The fluorescence of NADPH formed by G-6-PD was not interfered with by 6-PGD activity. This is a sensitive procedure which detects slight loss of G-6-PD in red blood cells and could be applied to the detection of G-6-PD deficiency.

Chromatography, DEAE-Cellulose↗
PubMed1988

Enzymatic diagnosis in non-spherocytic hemolytic anemia.

Blood samples from 722 unrelated patients with anemia and/or reticulocytosis were submitted to our laboratory for red cell enzyme assay during the past 7 years. Among these 722 cases, we found 82 cases of 7 different red cell enzyme deficiencies and 2 of unstable hemoglobin. Abnormalities of pyruvate kinase (PK) were found to cause hemolysis in 55 patients. Although their average PK activity was about 35% of the normal level, 5 showed normal and 2 demonstrated high PK activity. Among 17 patients in whom pyruvate kinase assays or screening tests had been carried out in routine laboratories, the correct diagnoses had been made in only 4. Glucose-6-phosphate dehydrogenase (G6PD) deficiency was found in 15 patients, pyrimidine 5'-nucleotidase deficiency in 5, glucose phosphate isomerase deficiency in 3, adenylate kinase deficiency in 2, phosphoglycerate kinase deficiency in 1, and glutathione synthetase deficiency in 1 patient. Even after we performed a panel of over 20 different red cell enzyme assays, 519 patients still remained undiagnosed.

Adolescent↗
PubMed1982

G6Pd Kanazawa: a new variant of glucose-6-phosphate dehydrogenase associated with congenital nonspherocytic hemolytic anemia.

A new variant of G6PD associated with chronic nonspherocytic hemolytic anemia (CNSHA) in a Japanese male is described. This variant is unique in that it has a normal electrophoretic mobility, normal Km for glucose-6-phosphate and NADP, and a normal utilization of the substrate 2-deoxyglucose-6-phosphate and deamino-NADP. It also shows a decreased thermal stability and a biphasic pH curve. These characteristics distinguish this variant from previously reported variants associated with CNSHA and we have called it G6PD Kanazawa.

Adult↗
PubMed1983

The effect of methyl oleate hydroperoxide, a possible toxic ozone intermediate, on human normal and glucose-6-phosphate dehydrogenase-deficient erythrocytes.

Erythrocytes of both normal and glucose-6-phosphate dehydrogenase (G-6-PD)-deficient humans responded in a dose-dependent manner to the oxidant stress of methyl oleate hydroperoxide (MOHP) as measured by decreases in G-6-PD activity, increases in methemoglobin (METHB) levels, and decreases in reduced glutathione (GSH). The G-6-PD-deficient erythrocytes displayed a markedly enhanced sensitivity to MOHP-induced decreases in G-6-PD activity and METHB increases while being less sensitive than normal erythrocytes to changes in GSH levels.

Erythrocytes↗
PubMed1989

Neonatal jaundice and glucose-6-phosphate dehydrogenase deficiency.

Ninety-six newborn aged 0-7 days with serum bilirubin of more than 15 mg/dl were studied for the G6PD status using semiquantitative and the assay method. It was found that the result of the 2 methods corresponded. The prevalence of G6PD deficiency was 12.4 per cent (there were 11 boys and one girl). Among the G6PD deficiency and the normal group, there was no difference in the age of the patient, onset of jaundice, bilirubin level, hematocrit status and the reticulocyte count. The semiquantitative method is a reliable as the assay method.

Bilirubin↗
PubMed1993

Frequency and clinical significance of erythrocyte genetic abnormalities in Omanis.

The frequencies of four malaria associated erythrocyte genetic abnormalities have been established in 1000 Omani subjects. They are: homozygous alpha+ thalassaemia (-alpha/-alpha) 0.45; high Hb A2 beta thalassaemia trait 0.015; sickle trait (Hb A/S) 0.061; and glucose 6 phosphate dehydrogenase deficiency (Gd-): males 0.27, females 0.11. From our data the alpha+ (-alpha/) thal gene (confirmed by Southern blotting) is pandemic in this population. Moreover, in spite of the very high frequency of Gd-, oxidative haemolytic syndromes are very uncommon. Also preliminary data indicate that among the Omani population with sickle cell disease, homozygosity of the alpha+ gene markedly modifies the clinical picture.

Adolescent↗