ArticleBioinformation2013
Insertion/Deletion polymorphisms do play any role in G6PD deficiency individuals in the Kingdom of the Saudi Arabia.
Article in Bioinformation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Deleterious effect of angiotensin-converting enzyme gene polymorphism in vitiligo patients.Saudi journal of biological sciences · 2021Article
- Insertion and deletion polymorphism in the alpha-2B adrenoceptor gene in pregnant women ripens gestational diabetes mellitus.Saudi journal of biological sciences · 2016Article
- Next generation sequencing (NGS) in glucose-6-phosphate dehydrogenase (G6PD) deficiency studies.Bioinformation · 2016Article
- Genetic polymorphisms in paraoxonase 1 and G protein-coupled receptor 77, and the risk of glucose-6-phosphate dehydrogenase deficiency in a Saudi population.Saudi medical journal · 2015Article
- Association of angiotensin converting enzyme gene insertion/deletion polymorphism and familial hypercholesterolemia in the Saudi population.Lipids in health and disease · 2013Article
- G6PD Enzyme Deficiency in Neonatal Pathologic Hyperbilirubinemia in Yazd.Iranian journal of pediatric hematology and oncology · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme in the pentose phosphate pathway (PPP) that plays an important role in protecting cells from oxidative damage by producing NADPH and reduced glutathione. G6PD deficiency is considered one of the most common genetic disorders present in the X chromosome and is the most common of enzymopathic red blood cell disorder. Angiotensin converting enzyme (ACE) plays an essential role in two physiological systems, one leading to the production of angiotensin II and the other to the degradation of bradykinin. Most studies focused on an insertion/deletion (I/D) polymorphism in intron 16 of the ACE gene as a marker for a functional polymorphism. The α(2B)-adrenergic receptor gene (α(2B)AR) is a three-amino acid deletion (12Glu9) polymorphism is located on chromosome 2. (Glu(9)/Glu(9)) of this polymorphism has been first time studies in G6PD individuals. We have selected 39 G6PD deficiency male individuals and PCR was carried out with the I/D polymorphisms. ACE I/D polymorphism study was carried out in G6PD individuals and showed strong association with DD genotypes and D alleles OR=39.38, p<0.0001 (95% CI=8.80-176.1) and OR=38.58, p<0.0001 (95% CI=13.21-112.6). Another gene of α(2B)AR I/D polymorphism study cannot show any association in DD genotype OR-0.6882,p=0.9388 (95% CI=0.2035-2.327) and with D allele OR-0.9614,p=0.9388 (95% CI=0.3482-2.653). Our study shows that G6PD deficiency is showing strong association in DD genotype and D allele of ACE gene and α(2B)AR gene have not shown any important role and one of the reason could be the low sample size.
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