Unfortunately, APAP toxicity in pregnancy can result in significant morbidity and mortality for both the mother and the fetus.46 APAP can freely cross the selective maternal-fetal barrier of the placenta, after which it can then be metabolized by fetal hepatocytes, causing fetal hepatic necrosis if appropriate therapy with NAC is not administered in a timely manner.47 Even though there is heightened activity of glucouronidation and oxidative pathways, causing the increased clearance of APAP in pregnancy, no evidence exists to suggest pregnancy as a predisposing risk factor for APAP toxicity.1 Moreover, despite that fact that APAP can cross the placental barrier, the only instances when the fetus has been shown to be at risk is when the mother suffers from severe APAP hepatotoxicity, which is usually apparent based on the history of presenting illness
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86 Notch signaling pathway Notch signaling, intimately involved in embryonic development and maintenance of multicellular organisms in adults, is activated by ligand-receptor interaction between adjacent cells, which leads to successive proteolytic cleavages and releases the notch intracellular domain (NICD)
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