Arachidonic acid release from tissue membranes and/or formation of free radical species have been considered to affect blood-brain barrier permeability and formation of brain oedema. To determine whether exogenous arachidonic acid or H2O2 may alter blood-brain barrier permeability, we examined their effect on cultured endothelium derived from cerebral microvessels of human and animals. Release of 51Cr from labeled endothelium exposed to these substance was used as a main marker for the assessment of endothelial injury. The results of these studies indicate that endothelial cells (EC) are susceptible to exogenous arachidonic acid or H2O2 insult irrespective of their origin. However human endothelial cells are less affected than animal EC by H2O2-generated systems. The findings suggest that a disturbance of the existing balance between the endogenous antioxidant properties of EC and exogenous oxidant leads to EC injury.
ASJC Scopus subject areas
- Clinical Neurology