Molecular Analysis of Glucose-6-Phosphate Dehydrogenase Gene Mutations in Bangladeshi Individuals

نویسندگان

  • Suprovath Kumar Sarker
  • Md Tarikul Islam
  • Grace Eckhoff
  • Mohammad Amir Hossain
  • Syeda Kashfi Qadri
  • A. K. M. Muraduzzaman
  • Golam Sarower Bhuyan
  • Mohammod Shahidullah
  • Mohammad Abdul Mannan
  • Sarabon Tahura
  • Manzoor Hussain
  • Shahida Akhter
  • Nazmun Nahar
  • Tahmina Shirin
  • Firdausi Qadri
  • Kaiissar Mannoor
چکیده

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common X-linked human enzyme defect of red blood cells (RBCs). Individuals with this gene defect appear normal until exposed to oxidative stress which induces hemolysis. Consumption of certain foods such as fava beans, legumes; infection with bacteria or virus; and use of certain drugs such as primaquine, sulfa drugs etc. may result in lysis of RBCs in G6PD deficient individuals. The genetic defect that causes G6PD deficiency has been identified mostly as single base missense mutations. One hundred and sixty G6PD gene mutations, which lead to amino acid substitutions, have been described worldwide. The purpose of this study was to detect G6PD gene mutations in hospital-based settings in the local population of Dhaka city, Bangladesh. Qualitative fluorescent spot test and quantitative enzyme activity measurement using RANDOX G6PDH kit were performed for analysis of blood specimens and detection of G6PD-deficient participants. For G6PD-deficient samples, PCR was done with six sets of primers specific for G6PD gene. Automated Sanger sequencing of the PCR products was performed to identify the mutations in the gene. Based on fluorescence spot test and quantitative enzyme assay followed by G6PD gene sequencing, 12 specimens (11 males and one female) among 121 clinically suspected patient-specimens were found to be deficient, suggesting a frequency of 9.9% G6PD deficiency. Sequencing of the G6PD-deficient samples revealed c.C131G substitution (exon-3: Ala44Gly) in six samples, c.G487A substitution (exon-6:Gly163Ser) in five samples and c.G949A substitution (exon-9: Glu317Lys) of coding sequence in one sample. These mutations either affect NADP binding or disrupt protein structure. From the study it appears that Ala44Gly and Gly163Ser are the most common G6PD mutations in Dhaka, Bangladesh. This is the first study of G6PD mutations in Bangladesh.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Molecular Identification of the Most Prevalent Mutations of Glucose-6-Posphate Dehydrogenase (G6PD) Gene in Deficient Patients in Khorasan Province of Iran

Glucose-6-phosphate dehydrogenase (G6PD) enzyme catalyses the first step in pentose phosphate pathway (conversion of glucose-6-phosphat to 6-phospho gluconat) which provides cells with pentoses and reduction power in the form of NADPH. In the present study we have analyzed the G6PD gene mutations in 76 patients with a history of favism in Khorasan province in Iran. DNA samples were analyzed for...

متن کامل

MOLECULAR IDENTIFICATION OF THE MOST PREVALENT MUTATION OF GLUCOSE-6-PHOSPHATE DEHYDROGENASE (G6PD) GENE IN DEFICIENT PATIENTS IN GILAN PROVINCE

Glucose-6-Phosphate Dehydrogenase (G6PD) is a cytosolic enzyme which its main function is to produce NADPH in the red blood cells by controlling the step from Glucose-6-Phosphate to 6-Phospho gluconate in the pentose phosphate pathway. G6PD deficiency is the most common X-chromosome linked hereditary enzymopathy in the world, that result in reduced enzyme activity and more than 125 different mu...

متن کامل

Molecular Identification of the Most Prevalent Mutation of Glucose-6-Phosphate Dehydrogenase Gene in Deficient Patients in Sistan and Balochestan Province of Iran

Glucose-6-phosphate dehydrogenase (G6PD) in humans is an X-chromosome-linked disorder and housekeeping enzyme, vital for the survival of every cell. It catalyses the oxidation of glucose-6-phosphate to 6-phospho gluconate in the first committed step of the pentose phosphate pathway, which provides cells with pentoses and reducing power in the form of NADPH. NADPH is required to protect the cell...

متن کامل

SPREAD OF THE GLUCOSE-6-PHOSPHATE DEHYDROGENASE VARIANT (G6PD-MEDITERRANEAN) IN ONE OF THE COASTAL PROVINCES OF CASPIAN SEA IN IRAN

In order to explore the nature of glucose-6-phosphate dehydrogenase (G6PD) deficiency in one of the coastal provinces of the Caspian Sea (Mazandaran) in Iran, we have analysed the G6PD gene in 74 unrelated G6PD-deficient males (2-6 year children) with a history of Favism, by using PCR and subsequent digestion by appropriate restriction enzymes, looking for the presence of certain known mutation...

متن کامل

Molecular Surveying of the Common Variants of Glucose 6-Phosphate Dehydrogenase Gene in Deficient Patients

Glucose 6-phoshphate dehydrogenase is X-chromosome linked that expressed in all tissues. This is the first enzyme of pentose phosphate pathway were 5-carbon sugar Ribose and NADPH were synthesized by coupled oxidation /reduction reactions and this enzyme is a highly polymorphic enzyme in humans. G6PD deficiency are shown to be the cause of haemolytic effect of Fava beans and primaquine. It soon...

متن کامل

Molecular Identification of the Most Prevalent Mutations of Glucose-6-Phosphate Dehydrogenase (G6PD) in Fars and Isfahan of Iran

Glucose-6-phosphate dehydrogenase (G6PD) in humans is in X-linked disorder, housekeeping enzyme and vital for the survival of every cell. It catalyses the oxidation of glucose-6-phosphate to 6-phospho Gluconat in the first committed step of the pentose phosphate pathway, which provides cells with pentoses and reducing power in the form of NADPH. NADPH is required to protect the cells against ox...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 11  شماره 

صفحات  -

تاریخ انتشار 2016