The conceptus requires zinc for normal growth and
development and is therefore at heightened risk when
the supply of zinc is suboptimal. Maternal zinc deficiency
can disrupt the normal function of trophoblast, the
embryonic-derived component of the placenta responsible
for implantation, production and secretion of
hormones, establishment of the maternal-fetal barrier
and the mediation of metabolic exchanges across this
barrier. The trophoblast is important for establishing
and maintaining the fetoplacental unit and trophoblastic
dysfunction has been linked to improper fetal development
and poor pregnancy outcomes including
spontaneous abortion, prolonged gestation, difficult
labor, low birth weight, and more complications during
delivery. Malformations associated with zinc deficiency
include abnormalities in brain and eye functions, audiometric
performance, cleft lip and palate, and
abnormalities of the heart, lung and urogenital systems.
Fetuses in zinc-deficient mothers often show growth
retardation, and a high frequency of skeletal abnormalities.
Biochemical and functional abnormalities can be
displayed in the lung and pancreatic systems. Evidence
that zinc deficiency is a teratogenic risk in humans
include (i) women with acrodermatitis enteropathica
tend to have complicated pregnancies if they do not
receive zinc supplements; (ii) low plasma zinc levels
have been associated with increased risk of malformations
and low birth weight; and (iii) several studies show that
zinc supplementation is associated with increased birth
The conceptus requires zinc for normal growth and
development and is therefore at heightened risk when
the supply of zinc is suboptimal. Maternal zinc deficiency
can disrupt the normal function of trophoblast, the
embryonic-derived component of the placenta responsible
for implantation, production and secretion of
hormones, establishment of the maternal-fetal barrier
and the mediation of metabolic exchanges across this
barrier. The trophoblast is important for establishing
and maintaining the fetoplacental unit and trophoblastic
dysfunction has been linked to improper fetal development
and poor pregnancy outcomes including
spontaneous abortion, prolonged gestation, difficult
labor, low birth weight, and more complications during
delivery. Malformations associated with zinc deficiency
include abnormalities in brain and eye functions, audiometric
performance, cleft lip and palate, and
abnormalities of the heart, lung and urogenital systems.
Fetuses in zinc-deficient mothers often show growth
retardation, and a high frequency of skeletal abnormalities.
Biochemical and functional abnormalities can be
displayed in the lung and pancreatic systems. Evidence
that zinc deficiency is a teratogenic risk in humans
include (i) women with acrodermatitis enteropathica
tend to have complicated pregnancies if they do not
receive zinc supplements; (ii) low plasma zinc levels
have been associated with increased risk of malformations
and low birth weight; and (iii) several studies show that
zinc supplementation is associated with increased birth
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