ØAs placenta matures, it changes from a hypoxic
environment to an oxygen-rich environment.
ØThis favours the production of reactive oxygen
species (ROS) which increases free iron concentration (Liochevand
Friedovich
1997).
Ø Nitric oxide is also locally
produced by the placenta (Dotsch
et al. 2001), and together with other reactive nitrogen species it contributes
to the potential OS in the presence of transitional metals.
Ø Macrophages infiltrate the
placenta resulting in the production of free radicals, including reactive
chlorine species.
Preeclampsia is a perinatal
disorder related to the OS taking place in the placenta.
placental ischaemia
results in OS characterised by an increase in levels of superoxide and lipid peroxidation
products and decrease in levels of
antioxidants, especially ascorbate.
These abnormalities result in endothelial dysfunction, considered
responsible for the clinical manifestations of the disease
Oxidative defence
mechanisms, such as superoxide
dismutase(SOD) activity in erythrocytes and plasma thiol
levels, were found to be lower in pregnant women than in non-pregnant women,suggesting
an oxidative environment and stress (Wisdom et al.1991).
Ø Serum levels of products of lipid peroxidation
increase in pregnant women, reaching their maximal concentrations in the second
trimester and then declining until term.
Ø However, levels similar to those in the
first trimester are observed in non-pregnant women, (Qanungo
and Mukherjea
2000).
•Transitional
metals, especially iron, which are particularly abundant in the placenta, are
important in the production of free radicals (Casanueva
and Viteri
2003).
•
Some studies have shown that iron may be related to the reduction of the
antioxidant capacity and to the increase in free radicals production and inflammatory
response.
•
However, there is a gap in the studies that show the involvement of iron metabolism and its
relationship with these possible metabolic processes present in pregnancy
Both localised and generalised
iron excess, and deficiency are situations where free radical damage has been
observed.
This can lead to functional
disturbances and foster genetic alterations.
A controversial issue,
researched by Lachili et al. (2001), is whether the
recommended doses of iron supplements taken during pregnancy can reduce OS, by correcting iron
deficiency, or increase it by creating a
condition of temporary iron overload.
Possible effects of vitamin C, when
consumed with iron, have to be taken into account in order to answer the above question.
•Elevated values of parameters of
OS were observed in complicated pregnancies. This supports the important role
of OS in diseases during pregnancy, particularly preeclampsia,diabetes
and preterm birth (Clerici
et al. 2012).
•Therefore,in
this study we tried to confirm the development of OS during pregnancy and to assess how iron and folic
acid contribute to OS.
MATERIALS AND
METHODS
v
50 pregnant and 25
non-pregnant age matched healthy
female Age : 21 – 40 years
v Written consent obtained after
informing purpose of study.
•Participants
and study design:
•Group A1 - < 35 years.
•Group A2 - ≥ 35 years.
•Group B1 – with iron
supplementation.
•Group B2 – with folic acid
supplementation.
•Group B3 – with iron and folic
acid supplementation
•Group B4 - no supplementation.
Sample
handle
blood samples collected from cubitus
vein at rest atleast
8 hr fasting ,about 8 am, in first trimester – 12 ± 2
weeks in third trimester – 34 ± 4
weeks.
Ø samples with EDTA assayed immediately
for hemoglobin and hematocrit.
Ø serum isolated after centrifugation
stored at -80⁰c for 1 month
before TAC determination.
Serum
TAC evaluation:
TAC assessed using antioxidant
assess kit of Cayman chemical Co..
- expressed in mmol/L.
ØStatistical
analysis:
- using statistical package for socialsciences
17.
- independent sample t test or Mann whitney
test used for normally and non-normally distributed values for comparing first
and third trimester
RESULT
•Table
I. TAC serum levels (mmol/l)
in all groups of women, expressed in
•median
(range).
•Groups
n
•TAC
serum levels ( mmol/l)
•Median
(minimum– maximum) p
•Control
group 25 3.34 (2.38 – 3.88) ∗
•1st
Trimester 3rd Trimester
•Study
group 50 2.1 (0.8 – 3.6) ∗ 3.02 (0.4 – 4.1)
0.0001
•A1 41
2.11 (0.8 – 3.6) ∗ ∗ 3.15 (0.4 – 4.1) ∗ ∗ ∗ 0.05
•A2 9
1.75 (1.1 – 3.4) ∗ ∗ 2.60 (1.8 – 3.3) ∗ ∗ ∗ 0.001
•B1 10 2.20 (1.4 – 3.2) 2.55 (0.8 –
3.4) 0.598
•B2 11 2.11 (1.1 – 3.4) 3.20 (1.8 –
3.6) 0.01
•B3 18 1.92 (1.1 – 3.2) 2.69 (1.75 –
4.1) 0.057
•B4 11 2.10 (0.8 – 3.6) 3.20 (0.4 –
3.65) 0.023
•TAC,
Total antioxidant capacity .
•∗ p 0.001; ∗ ∗ p
0.528; ∗ ∗ ∗ p 0.25.
•A1,
aged 35 years; A2, aged 35 years; B1, iron intake; B2, folic acid
intake; B3, iron
•and
folic acid intake; B4, no supplementation.
•J Obstet Gynaecol
Downloaded from informahealthcare.com by University of Bristol on 03/01/15
•For
personal
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