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. Author manuscript; available in PMC: 2021 Jul 8.
Published in final edited form as: Clin Perinatol. 2016 Feb 28;43(2):341–354. doi: 10.1016/j.clp.2016.01.010

Figure 3:

Figure 3:

Contribution of G6PD deficiency to bilirubin-induced neurotoxicity. (a) Neonatal jaundice results from production of bilirubin (shown as yellow hexagons) following hemolysis. In G6PD-normal infants, GSH levels are properly maintained and low levels of bilirubin-induced oxidative stress are safely neutralized. (b) In G6PD-deficient infants, higher levels of hemolysis lead to higher concentration of bilirubin in the brain, which inhibits mitochondrial activity (indicated by yellowed mitochondria). Reduced G6PD activity leads to low NADPH levels, and GSH is depleted in favor of GSSG. Buildup of ROS leads to neuroinflammation, cell death, and kernicterus. BBB; blood-brain-barrier