(GSH) in Pregnancy
® 2004 Priya Shah
Glutathione and Fertility
Glutathione and the Developing Fetus
Factors: Pollution, Toxins
• Pesticides and Persistent Organic
• Air pollution
• Heavy metal pollution (mercury,
• Vinyl chloride
• Excessive Oxygen: Hyperoxia
Drugs and Metabolites
Anti-psychotic and anti-epileptic drugs (AEDs)
factors: Smoking and Alcohol
• Alcohol (ethanol) consumption
Glutathione and Pregnancy Complications
Glutathione During Labor and Birth
• Infection and Inflammation
• Fetus with Cystic Fibrosis gene
stress and free radical formation can cause birth defects, abortion
and miscarriages in pregnancy. There is overwhelming evidence
to show that supplementation with glutathione precursors and antioxidants
protects the fetus and mother from the harmful effects of oxidative
stress in fertility, pregnancy, prececlampsia, diabetic pregnancy,
pregnancy complications, and preterm labor.
pregnancy is associated with an increase in oxidative stress and
lipid peroxidation, but antioxidant protection also increases.
Several of the antioxidants, such as vitamin E, increase progressively
with gestation, so there is a gradual favoring of antioxidant
activity over oxidative stress and lipid peroxidation (LOOH) as
normal pregnancy advances.
placenta, concentrations of the antioxidant enzymes, superoxide
dismutase and catalase, increase as gestation progresses, but
lipid peroxide concentrations decrease. Therefore, in normal pregnancy,
there is a sufficient increase in antioxidants to offset the increase
in peroxidation. (1)
the American College of Obstetrics and Gynecology advises all
pregnant women to take a prenatal vitamin containing antioxidants.
In addition, they advise eating lots of fresh fruits and vegetables,
the best sources of antioxidant protection.
and glutathione status play an important role in the development
and growth of the fetus, maintenance of a healthy pregnancy -
and even before pregnancy, in fertility and conception.
GLUTATHIONE AND FERTILITY
of a successful in vitro fertilization of the egg cell was shown
to depend on the activity of the selenium-containing antioxidant
enzyme GSHPx (glutathione peroxidase) in the follicular fluid.
of the in vitro maturation (IVM) medium with Cysteamine and beta-mercaptoethanol
was found to increase intracellular glutathione (GSH) content
in oocytes, decrease in peroxide levels within oocytes and improve
embryo development and quality. (4)
GLUTATHIONE AND THE DEVELOPING FETUS
of glutathione in the development of the foetus and placenta is
crucial. Glutathione (GSH) can control cell differentiation, proliferation,
and apoptosis - essential functions in the developing embryo.
Glutathione plays an important role in the development of organs
(organogenesis) and the embryo (embryogenesis).
have clearly shown how chemicals (like 2-nitrosofluorene and acetaminophen)
which modulate intracellular glutathione (GSH) and cysteine levels
cause developmental abnormalities (dysmorphogenesis) in the fetus.
explains why lower levels of glutathione activities (like those
caused by drugs and increased oxygen levels) during organogenesis,
may make the fetus more vulnerable to developmental damage. (8)
placenta, glutathione detoxifies pollutants before they reach
the developing child. Most substances or factors which cause birth
defects (teratogens) are known to exert their embryotoxic effects
because they cause oxidative stress. (9)
is sensitive to the toxic and teratogenic effects of chemicals
in the early embryonic stages, whereas it is sensitive to carcinogenic
effects during late fetal stages.
administered to the mother can be transferred through the placenta
and induce cancer in the fetus. Many potential carcinogens tend
to act as abortifacients and teratogens as well. Many carcinogens
are much more active in the fetus than in adults. (10,11)
evidence points to potential risks of delayed effects upon prenatal
exposure to chemicals. In fact, several systems (e.g., nervous,
excretory) show important developmental processes well after the
organogenetic period, up to the postnatal phase. So these would
also be sensitive to developmental toxicants.
ENVIRONMENTAL FACTORS: POLLUTION AND TOXINS
number of substances in the environment are known to be toxic
to the growing fetus. It is impossible to completely eliminate
exposure to many of them, because we inhale or ingest them through
polluted food, air and water.
these compounds exert their damaging effects through the production
of free radicals that lower glutathione levels. Glutathione, as
the master-antioxidant, plays an important protective role role
in detoxifying these chemicals and reducing their damaging effects
on the body.
glutathione status is sensitive to environmental pollution - as
a study of placental detoxifying activity in chemically polluted
or radioactively contaminated regions like the Ukraine has shown.
activity of glutathione transferase activity in the placenta correlated
with the increased frequency of complications during the pregnancy
and the delivery and with the worsening status of newborns. (12,13)
Pesticides and Persistent organic pollutants (POPs)
like lindane, deplete cysteine (CYS) and embryonic GSH, indicating
that the glutathione redox cycle plays a role in lindane embryotoxicity
in early organogenesis. (14)
exposure to a mixture of pesticides and polychlorinated biphenyls,
or persistent organic pollutants (POPs) - similar to those present
in the diet of Inuit people - was found to alter hepatic (liver)
gene expression in the mother and the fetus. These changes may
have functional implications during pregnancy. (15)
have found that increased exposure to nitrogen-oxidizing compounds
(NOx - a component of air pollutants) in polluted areas, was related
to significant rises in the levels of methemoglobin. (16)
may lead to hypoxia and hypoxemia in pregnant women. It has an
important influence on maternal health and placental and fetal
development and may lead to conditions like anemia, threatened
abortion/premature labor, and signs of preeclampsia, compared
with normal pregnancies. (17)
that maternal exposure to environmental oxidants can increase
the risk of pregnancy complications by stimulating the formation
of cell-damaging lipid peroxides and decreasing maternal antioxidant
Heavy metal (mercury, cadmium, arsenic) pollution
to high levels of methylmercury (MeHg) a known teratogen, has
been found to compromise fetal glutathione redox status. (23)
exposures of smoking and arsenic exposure (as a result of living
in a smelter area) have been associated with lower levels of reduced
glutathione and higher concentrations of lipid peroxides in maternal
blood, cord blood and placenta. (18)
exposure during critical stages of development has been associated
with exencephaly (a neural tube defect) and gross facial and limb
is an important defense against oxidative stress and heavy metal
toxicity. Removal of heavy metals (mercury, lead, cadmium) from
the body requires glutathione.
with the glutathione precursor, N-Acetyl-L-cysteine (NAC) during
the period of organogenesis can drastically reduce the severe
embryolethality induced by methyl mercuric chloride (MMC). (24)
constituent in the manufacture of polyvinyl chloride (PVC) products,
vinyl chloride is known to have genotoxic and carcinogenic effects.
is detoxified in the liver, where it is conjugated to glutathione
and excreted in the urine. Chronic exposure to vinyl chloride
may significantly deplete the glutathione pool and reduce the
defensive mechanisms of the body against subsequent attacks by
oxidative metabolites. (26,27)
(GSH) levels have been shown to significantly enhance the embryotoxic
effects of acrylonitrile. (28)
Excessive Oxygen: Hyperoxia
may be essential for life but a sudden rush during the early weeks
of pregnancy could spell death for a foetus. The amount of oxygen
foetuses receive triples between the eighth and 15th week of pregnancy.
cytotrophoblasts, which anchor the placenta in the womb and invade
the blood vessels to limit oxygen intake, dissipate at about eight
to 10 weeks, allowing more of the gas in. In pregnant women who
about to miscarry at that time, there is an excessive and early
onset of maternal blood flow.
resistance to oxygen toxicity in newborn animals of some species
has been associated with a rapid increase in antioxidants in lung
tissue. The failure to maintain sustained high levels of total
glutathione during hyperoxia might suggest that glutathione depletion
is a factor in the timing of death from oxygen toxicity in these
to researchers, diet rich in antioxidant vitamins such as vitamins
C and E could help protect the foetus from this sudden change
in their environment. (30)
XENOBIOTICS: DRUGS AND METABOLITES
placenta possesses a significant amount of glutathione S-transferase
(GST) capable of detoxification or activation of xenobiotics during
the critical organogenesis period in the fetus. (31)
angiotensin-converting enzyme inhibitors, indomethacin affect
the functional maturation of the kidney, while anticonvulsivants,
antiretroviral compounds, and benzodiazepines affect the brain
on exposure in utero. (32)
are known to cause birth defects in the growing fetus by generating
free radicals, and depleting GSH stores.
Anti-Psychotic and Anti-Epileptic Drugs (AEDs)
epilepsy (WWE) have a risk of bearing children with congenital
malformations that is approximately twice that of the general
population. Most antiepileptic drugs (AEDs) have been associated
with such risk.
and carbamazepine have been associated specifically with the development
of neural tube defects (NTDs), especially spina bifida. (33)
commonly used in women of childbearing age for epilepsy and other
indications, but studies have shown marked detrimental effects
of in utero AED exposure on behavioral neurodevelopment. Free
radicals and epoxides are thought to play a role in these congenital
(CPZ), cyclophosphamide, sodium valproate, phenobarbital, vigabatrin,
are all known to have teratogenic effects. (35,36,37,38,39,40)
glutathione is able to detoxify a number of reactive metabolites.
The FDA'S Division of Reproductive and Developmental Toxicology
(DRDT) plans to develop methods to measure embryonic concentrations
of glutathione and to test additional scavenging compounds to
determine if they are able to decrease carbamazepine-induced embryotoxicity.
is a teratogen that causes stunted limb growth (dysmelia) during
direct evidence to suggest that the teratogenicity of thalidomide
may involve free radical-mediated oxidative damage to embryonic
cellular macromolecules. Studies have confirmed that thalidomide-induced
oxidative stress in utero leads to phocomelia (flipper-like limbs).
inhibits the formation of new blood vessels (angiogenesis) in
the growing embryo by generating of toxic hydroxyl radicals. (43)
has been shown to cause species-specific GSH depletion in rat
and rabbit embryos treated in culture. Rabbit conceptuses displayed
lower GSH and cysteine levels and a greater propensity for thalidomide-induced
GSH depletion than in rat conceptuses, consistent with the greater
sensitivity of the rabbit to thalidomide teratogenicity. (44,45)
LIFESTYLE FACTORS: SMOKING AND ALCOHOL
and alcohol intake are avoidable substances that are known teratogens
in humans. Both are known to affect GSH stores adversely.
during pregnancy has been linked to a variety of adverse pregnancy
outcomes, including low birthweight, spontaneous abortion, and
infant death. Maternal exposure to environmental tobacco smoke
(ETS) negatively affects neonatal birth weight. (46)
during the first months of pregnancy induces morphologic changes
in the placenta, because of the acute sensitivity of the outer
layer of the first trimester placenta to oxygen-mediated damage.
has shown that a having a certain genotype of the enzyme, glutathione-S-transferase,
could affect the outcome of maternal exposure to ETS on neonatal
birth weight. (49)
have shown that components of tobacco smoke can reach the fetus,
and that human fetal tissues are capable of activating carcinogens
similar to those in tobacco smoke. This suggests that prenatal
exposure to maternal smoking could cause transplacental carcinogenesis
in humans, and that resulting tumours could occur in adulthood.
that are most often found associated with maternal smoking in
pregnancy or ETS exposure, are childhood brain tumours and leukaemia-lymphoma,
with risks up to two or greater. (53)
stopping smoking is the primary goal in pregnancy, chemoprevention
provides a complementary approach applicable to high risk individuals
such as current smokers and ex-smokers. Glutathione is known to
detoxify the nicotine and free-radicals contained in cigarette
smoke - even second hand smoke.
of studies have proved that N-Acetylcysteine (NAC), a precursor
of glutathione, has anti-genotoxic and anti-carcinogenic properties.
NAC protects from the genotoxicity of cigarette smoke and its
(NAC) is often administered to respiratory patients with histories
of exposure to cigarette smoke and atmospheric pollutants, which
are known to act as glutathione (GSH) depletors and as cancer
initiators and/or promoters. (56)
with NAC enhances detoxification mechanisms, either by stimulating
enzyme activities promoting glutathione formation or by reacting
with direct-acting mutagens and with the genotoxic metabolites
of procarcinogens. (57)
Alcohol (Ethanol) consumption
effects of the maternal consumption of alcohol on the fetus have
been recognized for centuries. Fetal alcohol syndrome is characterized
by pre and postnatal growth retardation, mental retardation, behavioral
deficits, and facial deformities.
of alcohol during critical stages of neural tube development are
harmful to both the central nervous system (CNS) and axial skeleton
formation in the fetus. Fetuses exposed in utero to ethanol have
an increased incidence of cleft lip and cleft palate. (58,59)
of alcohol to adult rats is known to decrease liver glutathione
(GSH) levels. In utero administration of alcohol has also been
shown to produce a decrease in GSH levels, as well as prenatal
growth retardation, and intrauterine death. (60)
mechanism(s) by which alcohol produces teratogenic effects on
the developing fetus are not well understood, but there is increasing
evidence that alcohol-induced liver damage may be associated with
increased oxidative stress.
ethanol depletes GSH and cysteine earlier in utero than in vitro,
maternal protective mechanisms allow embryos exposed in utero
to respond rapidly to chemical-induced oxidative stress. (61)
liver damage is associated with oxidative stress, but co-administration
of N-acetylcysteine (NAC) - a precursor of glutathione - effectively
provides protection from toxic liver damage by elevating intracellular
glutathione concentrations. (62)
GLUTATHIONE AND PREGNANCY COMPLICATIONS
complications and birth defects have been linked to oxidative
stress and free radical damage to the mother and fetus. Increased
lipid peroxidation and reduced antioxidant activity are associated
with pregnancy complications.
antioxidant system has been shown to play an important protective
role in reducing the effects of oxidative stress in pregnancy
and childbirth. Several complications during pregnancy have been
linked to poor glutathione levels. (63)
habitual abortion (HA) are found to have significantly lower levels
of antioxidants like GSH, vitamin A, E and beta carotene and higher
levels of lipid peroxidation. (64,65)
conditions like diabetes are known to cause birth defects, and
others like preeclampsia, cause complications in pregnancy. There
is evidence of decreased detoxifying or free radical scavenging
capacity in pregnancies complicated by preeclampsia and diabetes.
maternal total glutathione levels are found to be lower than in
normal pregnancy. Also, diabetic preeclamptics showed low total
glutathione levels as compared to preeclampsia and control. (66)
1. Gestational Diabetes
in pregnant women is a known teratogen. Fetal malformations (embryopathy)
resulting from maternal type 1 or type 2 diabetes is a well-established
phenomenon, with the risk of a birth defect in a diabetic pregnancy
being at least two and as much as six times higher than normal.
diabetes has the potential to adversely affect the development
of multiple organ systems, resulting in a wide range of congenital
malformations. Generally, the birth defects most commonly associated
with maternal diabetes are caudal regression, situs inversus,
kidney malformations, cardiac anomalies, and neural tube defects
in pregnancy is also known to cause deficits in learning and memory
in the offspring. (71)
maternal environment produces irreversible developmental retardation
in the embryo very early in gestation. More common congenital
malformations in infants of diabetic mothers occur before the
seventh week of gestation.
that any therapeutic intervention aimed at decreasing the incidence
of congenital malformations must be instituted during the critical
early period. (72)
with diabetes have abnormally high blood sugar levels, which means
their embryos also have high blood sugar levels. This excess blood
sugar produces damaging free radicals in the blood faster than
antioxidants can eliminate them in the underdeveloped embryo -
a process known as oxidative stress.
oxidative stress can cause birth defects. Oxidative stress also
disrupts the expression of specific genes in the embryo, and may
be a more common cause of birth defects in the babies of women
with and without diabetes than is currently appreciated.
stress in the fetus can lead to inhibition of the Pax-3 gene.
Embryos of mothers with diabetes have low levels of this gene
and three times more neural tube defects. This may explain the
genetic basis for neural tube defects that occur in diabetic pregnancies.
embryonic malformations have been linked to an increase in free
radical formation and depletion of intracellular glutathione (GSH)
in embryonic tissues. An excess of reactive oxygen species (ROS)
has been associated with the increased rate of congenital malformations
in experimental diabetic pregnancy.
studies have associated fetal birth defects (dysmorphogenesis)
and embryonic death (abortion/miscarriage) in diabetic pregnancies
with an increase in maternal and embryonic oxygen-free radicals
and oxidative stress. (76,77) The oxidation of embryonic proteins
by free radicals may be an important factor in causing birth defects
in diabetic pregnancies.
of dietary fat intake on glutathione peroxidase (GPx) activity
also suggests a potential link among diet, insulin resistance,
and antioxidant status during pregnancy. These factors may contribute
to the increased levels of lipid peroxidation and oxidative stress
during pregnancy as well. (87)
and impaired responsiveness of GSH-synthesizing enzyme to oxidative
stress during organogenesis may have important roles in the development
of embryonic malformations in diabetes. (74)
conditions in the mother damage the yolk sac endodermal cells
and alter GSH transport to the fetus. Embryonic GSH is reduced
as a result. This could reduce fetal protection against oxidative
stress in diabetic mothers. (75)
free radical eliminating system of the embryo is immature, it
may be particularly vulnerable to oxidative stress. Even with
good control of diabetes, the risk for neural tube and other birth
defects among women with diabetes is two to five times higher
than those without diabetes.
may, hence, be critical to preventing birth defects in babies
of women with diabetes. (78)
radicals-scavenging enzymes can reduce the embryotoxic effects
induced by diabetic conditions. Previous in vitro and in vivo
studies show that antioxidants can protect the embryonic development
in a diabetic environment. (79)
is the main defense against free radicals in embryonic tissues,
as it is in adult tissues (80). Treatment with dietary GSH has
a protective affect on kidney function in diabetics, and suggests
that dietary GSH treatment may reduce diabetic complications (81).
of multivitamin supplements during pregnancy may also reduce the
risk for birth defects among offspring of mothers with diabetes
(82). Vitamin C supplementation of the maternal diet can reduce
the rate of malformation in the offspring of diabetic rats. (83)
antioxidative treatment with vitamins E and C has also been shown
to decrease fetal malformation rate and improve the oucome of
the pregnancy by reducing oxygen radical-related tissue damage.
is a serious condition in pregnancy characterized by high blood
pressure, swelling in the hands and face, and protein in the urine.
It is considered a key cause of death in pregnant women, as well
as premature delivery.
pathophysiologic changes observed in preeclampsia suggest that
endothelial cell (the cells that form the lining of blood vessels)
dysfunction plays an important role in this disorder. The cause
and development of preeclampsia is thought to be related to increased
oxidative stress and increased vasoconstriction (narrowing of
to women with uncomplicated pregnancies, women with preeclampsia
have antioxidant activity that is markedly reduced by late gestation.
Maternal blood levels and placental tissue levels, of lipid peroxides,
and the production rates of lipid peroxides, are even further
increased in preeclampsia as compared with normal pregnancy. (88)
many deficiencies of antioxidants, the preeclamptic woman is not
able to effectively control her increase in oxidative stress and
lipid peroxidation. For women with preeclampsia, this could potentially
cause oxidative damage to the endothelial cells in blood vessels.
preeclampsia have significantly increased levels of serum iron
when compared with normally pregnant women, probably due to the
decrease in the iron-binding capacity of the blood and peroxide-stimulated
release of iron from hemoglobin.
metals, such as iron (Fe++, Fe+++) react with superoxide, hydrogen
peroxide, and lipid peroxides to produce strong oxidizing oxygen
radicals that produce oxidative damage and initiate lipid peroxidation.
of studies have indicated that enhanced superoxide generation
and impaired glutathione metabolism may be involved in the cause
and outcome of preeclampsia. (93)
lower ratios of free to oxidized cysteine, homocysteine, and cysteinylglycine
- indicative of oxidative stress - are found in women with preeclampsia
and cysteine levels, are normally lowered in pregnant women with
normal blood pressure. But in women with preeclampsia they were
comparable to levels in non-pregnant women, whereas glutathione
levels are lower.
suggest that in women with preeclampsia, glutathione use is higher
or its synthesis is disturbed. Glutathione might, hence, affect
the disease process and outcome of preeclampsia. (92)
total glutathione levels in maternal whole blood are found in
pregnancies complicated by preeclampsia and diabetes. In preeclampsia,
maternal total glutathione levels are lower than in normal pregnancy.
Also, diabetic preeclamptics showed low total glutathione levels
as compared to preeclampsia and control. (94)
that detoxiftying or free radical scavenging capacity is decreased
- in pregnancies complicated by preeclampsia, or the HELLP (hemolysis,
elevated liver enzymes, low platelets) syndrome. (95)
and diabetic preeclamptic women also show a significant fall in
vitamin E levels, suggesting that lipid peroxidation plays a role
in the pathogenesis of preeclampsia (97).
lipid peroxidation may play an important role in the preeclampsia
because of its potential to causing vascular endothelial cell
also compelling evidence that women with low levels of carotenoids
in their blood and placenta are much likelier to develop preeclampsia
than women whose levels were normal. Carotenoids are natural pigments
that act like antioxidants in protecting cells against free-radical
oxygen damage. (98)
factor alpha (TNF-), a cytokine produced by macrophages and many
other cell types, is significantly increased in preeclampsia and
has been shown to induce oxidative stress and cause secretion
of vasoconstrictors in human endothelial cells. (99)
of studies have found that supplementation with antioxidants is
beneficial in prevention of pre-eclampsia. Supplementation with
vitamins C and E may be beneficial in the prevention of pre-eclampsia
in women at increased risk of the disease.
In a study
published in the the Lancet, British researchers found that pregnant
women who took 1000 mg vitamin C and 400 IU vitamin E reduced
their risk of pre-eclampsia by 76%. (100,101,102,103)
Infection and Inflammation
and maternal systemic infections are proposed causes of preterm
labor. The resulting prematurity is associated with 75% of infant
mortality and 50% of long-term neurologic handicaps.
generated in large quantities during an inflammatory response
are associated with maternal and fetal GSH depletion, compromising
the fetus. Oxidative stress damages the fetus independent of prematurity.
inactivation of free radicals with N-acetylcysteine (NAC), an
antioxidant and glutathione (GSH) precursors, has been found to
improve the outcome of preterm deliveries associated with inflammation.
Fetus with Cystic Fibrosis gene
have shown that the chronic and excessive inflammation that characterizes
cystic fibrosis (CF) begins in utero.
state directly damages the tissues of the body, which in turn
primes the body for bacterial colonization as well as eventual
immunodeficiency. If one could lessen or even shut off the very
start of that inflammation which begins in utero, the CF infant
should have a better start in life.
the most important antioxidant in the body and a powerful mucolytic.
Glutathione is also an important regulator of inflammation. The
CFTR channel, which is missing or defective in CF persons, is
the main efflux route of cellularly-produced GSH.
very important, as the redox state of GSH in immune system cells
is the primary trigger of inflammation in the body. If GSH becomes
depleted in immune system cells, inflammation begins. This is
precisely what begins to happen in the CF body, and this is what
is hypothesized to be happening in utero.
that supplementation of the mother with GSH may tend to rectify
any GSH deficit that may start to develop in the immune system
cells of her fetus. This should serve to lessen or even shut off
the origin of fetal inflammation.
addition to all of the usual vitamins and minerals a pregnant
woman is asked to take, a woman who is pregnant with a fetus that
she knows or suspects to have CF might also consider supplementation
with both DHA and GSH.
with two nutritional supplements - DHA and GSH - may lessen or
even prevent the manifestations of CF that begin even in utero.
GLUTATHIONE DURING LABOR AND BIRTH
of studies have shown that glutathione (GSH ) is crucial in preventing
or minimising the oxidative stress that occurs during labor and
the birth process.
stress is implicated in diseases that are associated with prematurity
(such as retinopathy, cerebral palsy, intraventricular hemorrhage,
and necrotizing enterocolitis). Nonenzymatic antioxidant reserve
is the first line of defense against free radicals.
women who deliver at full term, the process of labor triggers
a compensatory increase of the nonenzymatic antioxidant reserve
in fetal red blood cells. This may act to protect against the
relative hyperoxia (excess oxygen exposure) that is experienced
by the full-term newborn infant at birth.
decreased fetal nonenzymatic antioxidant reserve in preterm labor
and delivery, would enhance the vulnerability to free radical
damage of the preterm neonate. (106)
or birth asphyxia/hypoxia (deprivation of oxygen supply to the
brain) in preterm deliveries and labor can lead to cerebral palsy,
respiratory distress syndrome, irreversible brain injury, and
permanent neurological and intellectual handicaps.
a rapid change occurs from a relatively hypoxic to a relatively
hyperoxic environment, especially during artificial ventilation,
with all the risks of ROS-formation. In the fetal-to-neonatal
transition, important circulatory and respiratory changes ensue
which lead to oxidative stress evidenced by changes in glutathione
correlation found between the antioxidant capacity of the mothers
and babies, suggests that supplementation with sulfur-containing
amino acids (methionine, cysteine) during pregnancy would improve
the antioxidant capacity of prematures.
studies have found that oral administration of N-Acetyl-Cysteine
(NAC), a glutathione precursor, to the pregnant mother partially
prevents the oxidative stress and change in hepatic GSSG that
occurs in the fetal-neonatal transition. (108)
is found to maintain normal lavage and lung tissue GSH levels
in preterm animals exposed to hyperoxia and prevents the changes
in lung mechanics associated with oxygen-induced lung injury.
E treatment of "any retinopathy" infants seemed to have
a positive effect against the development of Retinopathy of Prematurity.
An antioxidant cocktail (selenium + vitamin E) given to the high-risk
mothers (advanced age, smoking, pregnancy-induced hypertension)
before delivery might be useful in prevention of Retinopathy of
evidence indicates that antioxidants like Glutathione, Vitamin
C, and E are crucial to all stages of pregancy - from pre-conception
to fetal growth and development, to labor and post-natal development.
to protect the fetus from the damaging effects of pollutants,
carcinogens and teratogens, and provide protection against the
oxidative stress that is known to cause congenital malformations,
abortion and miscarriage.
studies have shown that glutathione and other antioxidants are
crucial in preventing oxidative stress in in pregnant women with
inflammation or disease conditions like diabetes and pre-eclampsia,
or in fetuses at risk for developing cystic fibrosis.
antioxidant supplementation can decrease the incidence of birth
defects and protect both mothers and the fetus from the damaging
and possibly fatal consequences of pregnancy complications.
Pregnant women and nursing mothers should avoid the use of supplementary
glutathione. Pregnant women must always consult their healthcare
provider before initiating any course of supplementation. Women
who are pregnant or nursing should discontinue all supplements
except as directed by their healthcare providers.
role of oxidative stress and antioxidants in preeclampsia
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May Cut Pregnancy Problem: Antioxidants may control dangerous
By Colette Bouchez; HealthScout Reporter
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