Glutathione S-transferase polymorphism of neonatal hyperbilirubinemia in Korean neonates

Kang, Chang Seok; Hong, Seung Su; Kim, Ji Sook; Kim, Eun Ryoung

doi:10.3345/kjp.2008.51.3.262

Cited by 5 publications

(9 citation statements)

References 22 publications

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“…ere might be delayed induction of these proteins. Because plasma GSTM1 and GSTT1 are produced mainly in the liver [37], a change in hepatic enzyme activity in response to inhalation of TDI might occur later in the circulation. e delayed response of GST proteins has been well demonstrated in diet studies.…”

Section: Discussionmentioning

confidence: 99%

Association of GSTM1 and GSTT1 Null Genotypes with Toluene Diisocyanate-Induced Asthma

Lee

Jeong

Kim

et al. 2022

Canadian Respiratory Journal

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Background. Toluene diisocyanate (TDI) causes occupational asthma by generating oxidative stress, leading to tissue injury and inflammation. Glutathione transferases (GSTs) are detoxifying enzymes that eliminate oxidative stress. We examined whether the genotypes of the GSTM1 and GSTT1 genes are associated with TDI-induced occupational asthma (TDI-OA). Methods. The study population consisted of 26 asthmatics with a positive response to the TDI challenge (TDI-PA) and 27 asthmatics with negative responses (TDI-NA). GSTM1 and GSTT1 null and wild-type genotypes were determined using multiplex PCR. The plasma GSTM1 and GSTT1 protein concentrations were determined using ELISA. Results. The GSTM1 null genotype was more frequent in the TDI-PA than in the TDI-NA (77.8 vs. 50.0%, OR = 3.5, p = 0.03 ), while the frequency of the GSTT1 null genotype tended to be higher in the TDI-PA than in the TDI-NA (59.3 vs. 42.3%, OR = 1.98, p = 0.21 ). When analyzed together, the GSTM1/GSTT1 null genotype was more frequent in the TDI-PA than in the TDI-NA (48.2 vs. 15.3%, OR = 6.5, p = 0.04 ). The decline in the FEV in 1 s after TDI challenge was higher with the GSTM1/GSTT1 null than the GSTM1 wild-type/GSTT1 null genotypes (24.29% vs. 7.47%, p = 0.02 ). The plasma GSTM1 level was lower with the GSTM1 null than with the GSTM1 wild-type genotypes both before (13.7 vs. 16.6 ng/mg, p = 0.04 ) and after (12.9 vs. 17.1 ng/mg, p = 0.007 ) the TDI challenge, while the GSTT1 level was not changed with either the GSTT1 null or wild-type genotype. Conclusions. The GSTM1 null genotype, but not GSTT1 alone, may confer susceptibility to TDI-OA. However, the genetic effect of the GSTM1 null genotype may be enhanced synergistically by the GSTT1 null genotype. The genetic effect of GSTM1 was validated in the plasma as the GSTM1 protein level. Therefore, the GSTM1 and GSTT1 genotypes may be useful diagnostic markers for TDI-OA.

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Section: Discussionmentioning

confidence: 99%

Association of GSTM1 and GSTT1 Null Genotypes with Toluene Diisocyanate-Induced Asthma

Lee

Jeong

Kim

et al. 2022

Canadian Respiratory Journal

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“…108 The full text of the Korean study was not reviewed as the article is written in Korean. 69 Three of the studies found no relationship between the GSTT1 Ã 0 gene and hyperbilirubinemia, 23,66,108 while the Korean study found that this gene was negatively associated with hyperbilirubinemia (odds ratio, 0.14; 95% confidence interval. 0.24-0.70; p ¼ 0.001).…”

Section: Glutathione S-transferase Null Mutations and Neonatal Hyperbmentioning

confidence: 98%

“…64 The GST-mu 1 (GSTM1) gene is the most common gene expressed in the liver, and GST-theta 1 (GSTT1) gene is expressed mainly in the liver and kidneys. 44,66,69,70 GSTalpha genes (GSTA1 and GSTA2) are expressed mainly in the liver and testes. 44,46 Noticeable interindividual variation in expression of these classes of genes exist in humans.…”

Section: Cytosolic Glutathione S-transferase In Hepatocytesmentioning

confidence: 99%

“…Three case-control studies have been conducted (Turkey, 66 South Korea, 69 and Thailand 23 ) and one prospective cross-sectional study (Egypt) 108 examining the relationship between GSTM1 Ã 0 and GSTT1 Ã 0 genes and hyperbilirubinemia in full-term neonates. Little information was available to confirm if the Egyptian study was indeed a prospective cross-sectional study.…”

Section: Glutathione S-transferase Null Mutations and Neonatal Hyperbmentioning

confidence: 99%

“…0.24-0.70; p ¼ 0.001). 69 Results from the four studies on the relationship between the GSTM1 Ã 0 gene and hyperbilirubinemia are inconsistent, ranging from positive to negative relationships (►Fig. 2).…”

Section: Glutathione S-transferase Null Mutations and Neonatal Hyperbmentioning

confidence: 99%

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Decreased Glutathione S-transferase Level and Neonatal Hyperbilirubinemia Associated with Glucose-6-phosphate Dehydrogenase Deficiency: A Perspective Review

Al-Abdi

2016

Amer J Perinatol

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Classically, genetically decreased bilirubin conjugation and/or hemolysis account for the mechanisms contributing to neonatal hyperbilirubinemia associated with glucose-6-phosphate dehydrogenase (G6PD) deficiency. However, these mechanisms are not involved in most cases of this hyperbilirubinemia. Additional plausible mechanisms for G6PD deficiency-associated hyperbilirubinemia need to be considered. Glutathione S-transferases (GST) activity depends on a steady quantity of reduced form of glutathione (GSH). If GSH is oxidized, it is reduced back by glutathione reductase, which requires the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH). The main source of NADPH is the pentose phosphate pathway, in which G6PD is the first enzyme. Rat kidney GSH, rat liver GST, and human red blood cell GST levels have been found to positively correlate with G6PD levels in their respective tissues. As G6PD is expressed in hepatocytes, it is expected that GST levels would be significantly decreased in hepatocytes of G6PD-deficient neonates. As hepatic GST binds bilirubin and prevents their reflux into circulation, hypothesis that decreased GST levels in hepatocytes is an additional mechanism contributing to G6PD deficiency-associated hyperbilirubinemia seems plausible. Evidence for and against this hypothesis are discussed in this article hoping to stimulate further research on the role of GST in G6PD deficiency-associated hyperbilirubinemia.

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Prenylated Flavonoids of Genus Epimedium: Phytochemistry, Estimation and Synthesis

et al. 2023

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Prenylated flavonoids are the chemotaxonomic markers of genus Epimedium. Icariin, epimedin A, B and C are the main bioactive principles found in Epimedium spp. The chemical and pharmacological studies of a good number of prenylated flavonoids isolated from Epimedium species are reported in literature but their biosynthetic pathways have been explored to a limited extent only and remained ambiguous for a long time. In this review, an in‐depth and extensive coverage of Epimedium prenylated flavonoids is reported from 2012 to 2022 using SciFinder database for literature retreival. The review covers occurrence, synthesis, biosynthesis and quantification of prenylated flavonoids of genus Epimedium.

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Glutathione S-transferase polymorphism of neonatal hyperbilirubinemia in Korean neonates

Cited by 5 publications

References 22 publications

Association of GSTM1 and GSTT1 Null Genotypes with Toluene Diisocyanate-Induced Asthma

Association of GSTM1 and GSTT1 Null Genotypes with Toluene Diisocyanate-Induced Asthma

Decreased Glutathione S-transferase Level and Neonatal Hyperbilirubinemia Associated with Glucose-6-phosphate Dehydrogenase Deficiency: A Perspective Review

Prenylated Flavonoids of Genus Epimedium: Phytochemistry, Estimation and Synthesis

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