Placental mitochondria as a source of oxidative stress in pre-eclampsia

Pre-eclampsia is a hypertensive disorder of human pregnancy that is a leading cause of premature delivery and fetal growth retardation. It is characterized by hypertension, reduced uteroplacental blood flow, proteinuria and oedema. Pre-eclampsia is associated with increased lipid peroxidation in the...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Placenta (Eastbourne) 1998-11, Vol.19 (8), p.581-586
Hauptverfasser: Wang, Y., Walsh, S.W.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Pre-eclampsia is a hypertensive disorder of human pregnancy that is a leading cause of premature delivery and fetal growth retardation. It is characterized by hypertension, reduced uteroplacental blood flow, proteinuria and oedema. Pre-eclampsia is associated with increased lipid peroxidation in the maternal circulation and in the placenta. Mitochondria are sources of oxygen radicals and are enriched with polyunsaturated fatty acids that are susceptible to peroxidation. Therefore, the mitochondria could be an important source of oxidative stress and lipid peroxidation. To study this, the level of lipid peroxidation in the mitochondrial fraction of placentae obtained from normally pregnant women ( n=8) and women with pre-eclampsia ( n=8) was examined. Placental tissues were homogenized and the mitochondrial fraction was isolated by ultracentrifugation. Mitochondrial lipid peroxides were estimated by malondialdehyde (MDA). NADPH and Fe ++ were used to stimulate lipid peroxidation. Superoxide dismutase (SOD) was used to inhibit superoxide radicals and mannitol to inhibit hydroxyl radicals. The following results were found: (1) MDA levels were significantly greater in the mitochondrial fraction isolated from pre-eclamptic placentae than from normal placentae (27.4 ± 3.0 versus 17.0 ± 1.8 nmol/g tissue, mean ± s.e., P
ISSN:0143-4004
1532-3102
DOI:10.1016/S0143-4004(98)90018-2