Published online Dec 15, 1996. doi: 10.3748/wjg.v2.i4.215
Revised: July 25, 1996
Accepted: October 10, 1996
Published online: December 15, 1996
AIM: To investigate the mechanisms leading to the disordered response to aging liver Kupffer cells (KCs).
METHODS: The effects of aging on KC membrane signal transduction and eicosanoid production and their management with vitamin E (VE) were assessed by measuring inositol phospholipid (PI) metabolism, intracellular calcium responses, and prostaglandin Ea-2 (PGEa-2) production in response to the inflammatory signals endotoxin (LPS) and platelet activating factor (PAF).
RESULTS: Aging resulted in a significant alteration in signal transduction of PAF as both PI turnover and calcium response were significantly reduced in the 18- and 24-mo old groups, compared with the 6 mo-old group. Aging significantly reduced PGEa-2 production in response to LPS. VE pretreatment resulted in an increased PI turnover, calcium response and PGEa-2 production.
CONCLUSION: The aging KCs have a disordered membrane phospohlipid function and VE is an effective modulator on it.