Endothelial degradation of extracellular lyso-phosphatidylcholine.

Formation of lysophospholipids, including lyso-phosphatidylcholine (lysoPC), is enhanced during oxidation of low-density lipoprotein, in ischaemic tissue and under inflammatory conditions. Besides being potentially cytotoxic, extracellular lysoPC induces changes in several properties of vascular endothelial cells. These include expression of endothelial adhesion molecules and interference with the endothelial production of nitrogen monoxide, prostacyclin and growth factors.

Circulating markers of oxidative stress are raised in normal pregnancy and pre-eclampsia.

Objective: To determine whether circulating markers of oxidative stress are elevated in pre-eclampsia when appropriate precautions are taken to prevent in vitro oxidation

Design: A prospective study.

Setting: Nuffield Department of Obstetrics and Gynaecology, Oxford and The William Harvey Institute, London.

Sample: Three groups of women: those with pre-eclampsia (n = 19), control pregnant women (n = 19) matched for gestation, age and parity and a group of non pregnant individuals of reproductive age (n = 7).

Serum from preeclamptic women induces vascular cell adhesion molecule-1 expression on human endothelial cells in vitro: a possible role of increased circulating levels of free fatty acids.

Objective: The object was to determine whether serum from preeclamptic women induces expression of vascular cell adhesion molecule-1 on cultured endothelial cells.

Study Design: Endothelial cells were incubated with medium containing 20% serum (volume/volume) either from women with preeclampsia (n = 15) or from women with normal pregnancies (n = 15) matched for maternal age, gestational age, and parity. A further matched set of samples (n = 10) was exposed to endothelial cells that had previously been incubated in the presence or absence of vitamin E (40 micromol/L final concentration).

Large intravenous bilirubin loads increase the cytotoxicity of bile and lower the resistance of the canalicular membrane to cytotoxic injury and cause cholestasis in pigs.

Background: Large intravenous bilirubin loads cause loss of hepatic canalicular membrane microvilli and cholestasis. This study examines whether these untoward effects might be due to canalicular membrane injury from cytotoxic bile.

Methods: The cytotoxicity of bile was assayed against pig erythrocytes before and throughout 4.