Glutathione S-Transferase Gene Polymorphisms in Neonatal Hyperbilirubinemia

Ghany, Eman Abdel Ghany Abdel; Hussain, Nouran Fahmy; Botros, Shahira K. A.

doi:10.2310/jim.0b013e318235479a

Cited by 13 publications

(7 citation statements)

References 18 publications

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“…Other studies have also suggested that oxidative stress is the mediator of neurotoxic effect of bilirubin (46). It has been shown that neonate carriers of GSTM1-null genotype are at high risk to develop pathologic hyperbilirubinemia and may have higher bilirubin levels (47). Glutathione S-transferases can act as intracellular binding proteins for nonsubstrate ligands, including bilirubin and bilirubin conjugates, thus decreasing the efflux of bilirubin into plasma.…”

Section: Discussionmentioning

confidence: 99%

Autism Spectrum Disorders and Perinatal Complications—Is Oxidative Stress the Connection?

et al. 2019

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Background: Autism spectrum disorders (ASD) are complex psychiatric disorders, with gene environment interaction being in the basis of their etiology. The association of perinatal complications and ASD is well established. Recent findings suggested that oxidative stress and polymorphism in genes encoding antioxidant enzymes might be involved in the development of ASD. Glutathione transferases (GSTs) have an important role in the antioxidant defense system. We aimed to establish whether the predictive effects of prenatal and perinatal complications (as possible oxidative stress inducers) on ASD risk are dependent on GST polymorphisms. Methods: The study included 113 ASD cases and 114 age- and sex group-matched healthy controls. All participants were genotyped for GSTA1, GSTM1, GSTT1, and GSTP1 polymorphisms. The questionnaire regarding prenatal and perinatal risk factors and complications was administered for all the subjects in the study. Results: The evaluated perinatal complications as a group significantly increased the risk of ASD [odds ratio (OR) = 9.415; p = 0.000], as well as individual perinatal complications, such as prematurity (OR = 11.42; p = 0.001), neonatal jaundice (OR = 8.774; p = 0.000), respiratory distress syndrome (OR = 4.835; p = 0.047), and the use of any medication during pregnancy (OR = 2.413; p = 0.03). In logistic regression model, adding GST genotypes did not modify the significant effects found for prematurity and neonatal jaundice as risk factors in ASD. However, there was a significant interaction of GST genotype with medication use during pregnancy and the use of tocolytics during pregnancy, which was predictive of ASD risk only in carriers of GSTM1-null, as opposed to carriers of GSTM1-active genotype. Conclusion: Specific perinatal complications may be significant risk factors for ASD. GSTM1 genotype may serve as a moderator of the effect of some prenatal factors on the risk of ASD such as using medication during pregnancy. It may be speculated that different oxidative stress-related genetic and environmental factors could lead to development of ASD. Apart from etiological mechanisms, possible therapeutic implications in ASD are also discussed.

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Section: Discussionmentioning

confidence: 99%

Autism Spectrum Disorders and Perinatal Complications—Is Oxidative Stress the Connection?

et al. 2019

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“…However, in this study, the authors suggest that the null GSTM1 genotype may affect ligandin functions in hepatocytes, which are important in bilirubin transportation and therefore, patients with the null GSTM1 genotype might have elevated levels of bilirubin [ 53 ]. Abdel Ghany et al also demonstrated that the null GSTM1 variant represents a higher risk of developing hiperbilirubinemia in neonates [ 56 ]. However, in the present study, no statistically significant association was found between null the GSTM1 variant and bilirubin levels.…”

Section: Discussionmentioning

confidence: 99%

Sickle Cell Anemia Patients in Use of Hydroxyurea: Association between Polymorphisms in Genes Encoding Metabolizing Drug Enzymes and Laboratory Parameters

et al. 2018

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This study investigated associations between SNPs in genes encoding metabolizing drug enzymes and laboratory parameters in sickle cell anemia patients under hydroxyurea (SCA-HU+). We evaluated hematologic and biochemical parameters by electronic methods and SNPs by PCR-RFLP and multiplex PCR in 35 SCA-HU+ patients and 67 SCA-HU− patients. The HbS, total cholesterol, lactate dehydrogenase, aspartate aminotransferase, total bilirubin and fractions levels, and leukocyte, eosinophil, monocyte, and erythroblast counts were reduced in SCA-HU+ patients (p < 0.05). Moreover, they presented higher HbF, C-reactive protein, and ferritin levels and elevated MCH and MCV values (p < 0.05). Genotype frequencies of variants GA + AA of MPO −463G>A and c1c2 + c2c2 of CYP2E1 −1293G>C/−1053C>T were higher in SCA-HU+ patients (p < 0.05). Independent associations were found between the variant A allele and lower total cholesterol, between c2 allele and low alpha-1 antitrypsin and between the null GSTT1 variant and high indirect and total bilirubin in SCA-HU+ patients. In SCA-HU− patients, independent associations were found between the variant A allele and high uric acid and between c2 allele and high urea. Our results suggest that SNPs MPO −463G>A, CYP2E1 −1293G>C/−1053C>T, and GSTT1 can be associated with alterations in lipid, inflammatory, renal, hemolytic, and hepatic profiles. However, further studies are needed to elucidate these associations.

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“…Chen et al [24] reported that PBREM and A(TA)7TAA had high linkage disequilibrium among Chinese adults, and functional studies indicated that the combination of PBREM and A(TA)7TAA decreases the expression of UGT1A1 gene. [25] More detailed UGT1A1 genetic sequencing including PBREM and large insertion/deletion, and sequencing for other genes that were reported to cause UCH, such as solute carrier organic anion transporter family member 1B1 (SLCO1B1), [26,27] glucose-6-phosphate dehydrogenase (G6PD), [28] and Glutathione S-transferases (GSTs) [29,30] may shed some light into this phenomenon. Future studies should focus on genetically unexplained UCH cases and find plausible disease causing mechanisms.…”

Section: Discussionmentioning

confidence: 99%

UGT1A1 genotypes and unconjugated hyperbilirubinemia phenotypes in post-neonatal Chinese children

Abuduxikuer

Fang

et al. 2018

Medicine

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Glutathione S-Transferase Gene Polymorphisms in Neonatal Hyperbilirubinemia

Abstract: Neonates with the GSTM1 null genotype are at high risk to develop pathologic hyperbilirubinemia and may have higher bilirubin levels.

Cited by 13 publications

References 18 publications

Autism Spectrum Disorders and Perinatal Complications—Is Oxidative Stress the Connection?

Autism Spectrum Disorders and Perinatal Complications—Is Oxidative Stress the Connection?

Sickle Cell Anemia Patients in Use of Hydroxyurea: Association between Polymorphisms in Genes Encoding Metabolizing Drug Enzymes and Laboratory Parameters

UGT1A1 genotypes and unconjugated hyperbilirubinemia phenotypes in post-neonatal Chinese children

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