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Compared with other organs, the brain is more vulnerable to oxidative stress because its high consumption of oxygen generates large amounts of reactive oxygen species (ROS) and its lower antioxidant enzyme (glutathione peroxidase, catalase) activity and richness in polyunsaturated fatty acids (PUFAs) makes it highly susceptible to lipid peroxidation [43]
OXIDATION TOXIC PATHWAY (CYP2E1 enzyme) Only 5-10% of acetaminophen in healthy non-pregnant adults INCREASES by 80% during pregnancy[] Creates NAPQI (N-acetyl-p-benzoquinone imine)the toxic metabolite NAPQI formation 43% HIGHER in first trimester[] NAPQI must be immediately neutralized by glutathione When glutathione is depleted, NAPQI causes cellular damage Crosses the placenta and damages fetal brain HOW PREGNANCY CHANGES ACETAMINOPHEN METABOLISM METABOLIC PATHWAY CHANGES DURING PREGNANCY[] Human pharmacokinetic studies reveal dramatic shifts in how pregnant women metabolize acetaminophen: Oxidation to NAPQI (Toxic Pathway) INCREASES by 80% The Brookhuis et al
Data are presented as mean SD, n = 5 ( b ) biologically independent samples or median SE Median ( d ) calculated as the median abundance of detected lysophospholipid species divided by the median abundance of corresponding phospholipid species for each condition
Phagocytosis in atherosclerosis: Molecular mechanisms and implications for plaque progression and stability
There are at least three inborn errors in the pentose phosphate pathway that have been identified
