Correlation between oxidative stress and G6PD activity in neonatal jaundice

Area of Science:

• Biochemistry
• Neonatalogy
• Perinatal Medicine

Background:

• Fetal distress compromises oxygen supply, potentially leading to oxidative stress.
• Glucose 6-phosphate dehydrogenase (G6PD) deficiency can exacerbate oxidative stress and hemolysis.
• Neonatal jaundice is associated with altered oxidant-antioxidant profiles.

Purpose of the Study:

• To investigate oxidative stress markers in neonates with and without fetal distress.
• To assess the relationship between fetal distress, G6PD activity, and oxidative status.
• To evaluate red blood cell count and bilirubin levels in neonates with fetal distress.

Main Methods:

• Comparative study of 22 neonates with fetal distress and 24 controls.
• Analysis of umbilical cord blood for erythrocyte count, total bilirubin, G6PD activity, and oxidative stress parameters (TBARS, NO, O2(-), H2O2, SOD, CAT).
• Measurements performed at birth and hospital discharge.

Main Results:

• Neonates with fetal distress showed significantly higher levels of superoxide radicals (O2(-)), hydrogen peroxide (H2O2), superoxide dismutase (SOD), and related ratios (O2(-)/SOD, H2O2/CAT).
• Lower red blood cell counts and higher bilirubin levels were observed in neonates with fetal distress.
• Reduced G6PD and catalase (CAT) activity were noted in neonates experiencing fetal distress.

Conclusions:

• Fetal distress is associated with elevated oxidative stress markers and compromised antioxidant defenses in newborns.
• The findings suggest a complex interplay between fetal distress, G6PD activity, and oxidative imbalance, though the primary cause (oxidative stress vs. low G6PD) requires further elucidation.