TAUROCHOLATE INDUCES PREFERENTIAL RELEASE OF PHOSPHATIDYLCHOLINE FROMRAT-LIVER CANALICULAR VESICLES

Aims/Background: Biliary phospholipid secretion involves predominant s egregation of canalicular phosphatidylcholine into bile. We tested the hypothesis that micellar concentrations of the major physiologic bile salt taurocholate can preferentially solubilize phosphatidylcholine f rom the canalicular rat liver plasma membrane. Methods. Subcellular fr actions from rat liver and kidney were isolated with standardized proc edures, incubated in vitro with taurocholate or lamidopropyl)dimethyla mmonio]-propane-1-sulphonate (CHAPS) and released phospholipids determ ined after centrifugation. Results. After incubation of canalicular (c LPM) and basolateral (blLPM) rat liver plasma membrane vesicles with 6 and 8 mM taurocholate, the proportion of phosphatidylcholine released was about two-fold higher as compared with its relative contribution to the overall lipid composition of the membranes. Quantitatively, thi s taurocholate-induced preferential phosphatidylcholine release was ab out four-fold higher in cLPM (117 nmol) as compared with blLPM (28 nmo l). Comparison of membranes from different organs showed that increase d sphingomyelin content reduced taurocholate-induced phosphatidylcholi ne release. Furthermore, phosphatidylcholine release from cLPM did not fit an inverse exponential relationship between membrane sphingomyeli n content and phosphatidylcholine release from different starting mate rial, indicating that cLPM is especially prone to taurocholate-induced phosphatidylcholine release. In contrast, in rat liver microsomes and kidney brush border membranes, taurocholate released phospholipids in proportion of their membrane contents, indicating an unspecific membr ane solubilizing effect only. Similarly, CHAPS had an unselective lipi d solubilizing effects in cLPM and blLPM. Conclusion: These results su pport the concept that the very last step of canalicular phospholipid secretion is mediated in vivo by bile salt-induced vesiculation of pho sphatidylcholine-enriched microdomains from the outer leaflet of cLPM.