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From the Department of Obstetrics and Gynaecology,*
Chang Gung Memorial Hospital, Taipei, Taiwan; and the Department of
Anatomy,
University of Cambridge, Cambridge,
United Kingdom
Oxidative stress is a prominent feature of the placenta
in many complications of pregnancy, such as preeclampsia. The
cause is primarily unknown, although ischemia-reperfusion
injury is one possible mechanism. Our aim was to test this hypothesis
by examining the oxidative status of human placental tissues during
periods of hypoxia and reoxygenation in vitro. Rapid
generation of reactive oxygen species was detected using the
fluorogenic probe, 2',7'-dichlorofluorescein
diacetate, when hypoxic tissues were reoxygenated. The
principal sites were the villous endothelium, and to a lesser
extent the syncytiotrophoblast and stromal cells. Increased
concentrations of heat shock protein 72, nitrotyrosine
residues, and 4-hydroxy-2-nonenal were also observed in the
villous endothelial and underlying smooth muscle cells, and in
the syncytiotrophoblast. Furthermore, preloading placental
tissues with the reactive oxygen species scavengers desferrioxamine and
-phenyl-N-tert-butylnitrone reduced
levels of oxidative stress after reoxygenation. These changes are
consistent with an ischemia-reperfusion injury, and mirror
those seen in preeclampsia. Consequently, in
vitro hypoxia/reoxygenation may represent a suitable model
system for investigating the generation of placental oxidative stress
in preeclampsia and other complications of pregnancy.
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