Cross-linking of SH-groups in the erythrocyte membrane enhances transbilayer reorientation of phospholipids. Evidence for a limited access of phospholipids to the reorientation sites.

Oxidation of erythrocyte membrane SH-groups and concomitant cross-linking of spectrin, which induce a partial loss of phospholipid asymmetry (Haest, C.W.M., Plasa, G., Kamp, D. and Deuticke, B. (1978) Biochim. Biophys. Acta 509, 21-32) are now shown to result in a remarkable increase of the rates of transbilayer reorientation of exogenously incorporated lysophospholipids. Reorientation of both, neutral lysophosphatidylcholine and of negatively charged lysophosphatidylserine is enhanced. A decrease of the activation energy of the reorientation process as well as quantitative changes of the dependence of reorientation on the lysophosphatidylcholine and cholesterol content of the membrane indicate formation of new reorientation sites or modification of existing sites. A common mechanism may underly the formation of reorientation sites and the occurrence of leaks for small solutes (Deuticke, B., Poser, B., Lütkemeier, P. and Haest, C.W.M. (1983) Biochim. Biophys. Acta 731, 196-210) subsequent to oxidation of membrane SH-groups. Whereas exogenous lysophospholipids completely equilibrate between the two lipid layers regardless of the extent of oxidation of SH-groups, endogenous inner layer phospholipids become available for reorientation in a graded way. Native phospholipid asymmetry is therefore not the result of a low transbilayer mobility of phospholipids, but probably due to a lack of access of inner layer phospholipids to the reorientation sites.