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Updated: Mar 17, 2026

Spectrophotometric Screening for Potential Inhibitors of Cytosolic Glutathione S-Transferases
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Decreased Glutathione S-transferase Level and Neonatal Hyperbilirubinemia Associated with Glucose-6-phosphate

Sameer Yaseen Al-Abdi1

  • 1Department of Pediatrics, King Abdulaziz Hospital, Ministry of National Guard, Al-Ahsa, Saudi Arabia.

American Journal of Perinatology
|July 28, 2016
PubMed

Insights

Glucose-6-phosphate dehydrogenase (G6PD) deficiency may cause neonatal hyperbilirubinemia through decreased hepatic glutathione S-transferases (GST). This study explores GST

Area of Science:

  • Biochemistry
  • Neonatal Medicine
  • Genetics

Background:

  • Neonatal hyperbilirubinemia is often associated with glucose-6-phosphate dehydrogenase (G6PD) deficiency.
  • Traditional explanations (bilirubin conjugation, hemolysis) do not account for most cases.
  • Alternative mechanisms contributing to hyperbilirubinemia in G6PD deficiency require investigation.

Purpose of the Study:

  • To propose and discuss the hypothesis that decreased hepatic glutathione S-transferases (GST) activity contributes to neonatal hyperbilirubinemia in G6PD deficiency.
  • To explore the role of the pentose phosphate pathway, G6PD, and glutathione metabolism in this context.
  • To review evidence supporting and refuting the proposed GST mechanism.

Main Methods:

  • Literature review and theoretical analysis.
  • Examination of the relationship between G6PD, NADPH, glutathione (GSH), and GST activity.
  • Discussion of the correlation between G6PD levels and GST activity in relevant tissues (rat kidney/liver, human RBCs).
  • Hypothesizing the impact of decreased hepatic G6PD on hepatocyte GST levels and bilirubin metabolism.

Main Results:

  • G6PD is the rate-limiting enzyme in the pentose phosphate pathway, crucial for NADPH production.
  • NADPH is essential for regenerating reduced glutathione (GSH), which is required for GST activity.
  • Positive correlations observed between G6PD levels and GST activity in various tissues suggest a link.
  • It is hypothesized that G6PD deficiency leads to decreased hepatic GST, impairing bilirubin binding and increasing circulation.

Conclusions:

  • Reduced hepatic GST activity due to G6PD deficiency is a plausible additional mechanism for neonatal hyperbilirubinemia.
  • This hypothesis warrants further investigation to elucidate the precise role of GST in G6PD-related hyperbilirubinemia.
  • Understanding this mechanism could lead to improved management strategies for affected neonates.

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