Advanced glycation end products stimulate an enhanced neutrophil respiratory burst mediated through the activation of cytosolic phospholipase A2 and generation of arachidonic Acid.

Background: Advanced glycation end products (AGEs) enhance NADPH oxidase, and hence respiratory burst activity, of stimulated neutrophils. They are thus potentially vasculopathic, especially in diabetes, uremia, and aging, in which AGEs classically accumulate. We investigated the underlying mechanisms.

NADPH oxidase activity in preeclampsia with immortalized lymphoblasts used as models.

Upon activation, neutrophils release reactive oxygen species that are believed to contribute to the widespread manifestation of preeclampsia. Neutrophils have an NADPH oxidase enzyme that catalyzes the production of reactive oxygen species. Little is known about the manifestations of the activated response and the upstream signaling pathways that regulate this process in preeclampsia.

Neutrophil activation and production of reactive oxygen species in pre-eclampsia.

Objective: To investigate neutrophil NADPH oxidase activation and subsequent production of reactive oxygen species (ROS) in pre-eclampsia.

Design: Baseline values and the activated response of neutrophils upon stimulation of the NADPH oxidase with the agonists was measured. Neutrophils from 17 third-trimester pre-eclamptic and 17 age- and gestation-matched normal pregnant women were examined.