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Isolated mononuclear leukocytes, when incubated with purified haemoglobin Ao (HbAo), release the pro-inflammatory cytokines interleukin-8 (IL-8) and tumor necrosis factor-? (TNF-?). Thus, inflammation is believed to play a role in preeclampsia. Leukocytes increase due to inflammatory response. There is also increased hemoglobin production in the PE placenta. The hemoglobin may be released into the placenta blood vessel lumen. In addition, Gene and protein profilingstudies have shown increased expression and accumulation of free fetal hemoglobinin the preeclamptic placenta. Predominantly due to oxidative damage to the placentalbarrier, fetal hemoglobin leaks over to the maternal circulation. Oxidative stress in general, and more specifically fetal hemoglobin-inducedoxidative stress, could play a key role in the pathology of preeclampsia seen both in theplacenta and ultimately in the maternal endothelium.

Oxygen deprivation, or hypoxia, during pregnancy poses a multifaceted challenge to maternal and fetal well-being, significantly impacting gestational outcomes. This comprehensive review endeavors to elucidate the intricate mechanisms and consequences of hypoxia on maternal health within the context of pregnancy. Through an exploration of the complex interplay between oxygen insufficiency, placental function, and maternal physiology, this review aims to unravel the far-reaching implications of hypoxia on pregnancy outcomes. The discourse encompasses the pivotal role of hypoxia in precipitating various pregnancy complications such as preeclampsia, gestational hypoxia, and intrauterine growth restriction (IUGR), shedding light on their underlying pathophysiological processes and potential therapeutic avenues. By synthesizing current knowledge, this review aims to advance our comprehension of hypoxia\'s impact on maternal health during gestation, fostering the development of targeted interventions to alleviate adverse outcomes associated with oxygen deprivation in pregnancy.