Regional distribution of superoxide dismutase activity in human placenta and its correlation with lipid peroxidation

Abstract EN

The objectives of the present study are to determine the activity of superoxide dismutase (SOD) in various regions of human placenta, and to correlate this activity with lipid peroxidation.

To follow up changes in SOD activity and lipid peroxidation during gestation, a female rat model was used and pregnant females were sacrificed at 4, 7, 10, 14, and 18 days of gestation.

Placentas were collected from 45 uncomplicated term pregnancies.

Each placenta was sampled in 3 regions on the maternal and fetal side : central ; mid placenta ; and periphery.

5 gm of tissue were obtained for analysis and full thickness samples were obtained from the umbilical cord.

In the rat, 2-3 placentas from each (female (n=4) were pooled and assayed while the cord for all placentas of the same female were pooled and assayed.

The results show slight regional variations in the amount of lipid peroxidation as estimated by malondialdehyde (MDA) with the mid placental region of the fetal side being significantly higher than any of the other placental regions.

MDA concentration in the placenta and umbilical cord of female rat progressively increased with progress of gestation (67% increase in the placenta and 90% increase in the umbilical cord).

The results also show slight regional variations in SOD activity in the placenta being higher at the fetal site.

The SOD activity in the umbilical cord was significantly higher than any of the placental regions.

SOD activity in the placenta and umbilical cord of female rat progressively increased with the progress of gestation and after 10 days SOD activity in the umbilical cord was significantly higher than the placenta.

The results clearly show that the increase of lipid peroxidation in the placenta and umbilical cord during gestation is coupled with an increase in SOD activity.

The magnitude of SOD activity increase is higher to compensate for the increase in lipid peroxidation.