Neurochemical Research (3) 725-731 (1978) A POSSIBLE MECHANISM FOR CHOLESTERYL ESTER FORMATION DURING DEMYELINATION Lecithin" Cholesterol Acyltransferase (LCAT) Activity in Rat Brain L. AMADUCCI, 1 P. ANTUONO, 1 L. BARTOLINI, t G. E. DE MEDIO, 2 D. INZrrARI, 1 AND G. PORCELLATI z 1 Neurological Clinic, University of Florence, 50138 Florence, Italy, and 2 Department of Biochemistry, The Medical School, University of Perugia, 06100 Perugia, Italy Accepted April 24, 1978 Lecithin:cholesterol acyltransferase (LCAT) activity has been examined in the rat by using a brain homogenate preparation as the phospholipid substrate and blood plasma as the enzyme source. LCAT activity was detected on using 60/~1 of serum onwards. Successive experiments have also shown that LCAT activity is present in the edematous rat brain tissue homogenate when incubated with inactivated rat plasma as substrate. The results are discussed in relation to cholesteryl ester accumulation in brain during demyelinating diseases. INTRODUCTION Many authors indicate the action of cathepsins and phospholipase release from infiltrating cells (1) as the major cause of demyelination and cho- lesteryl ester formation in brain (2-4). However, often cholesteryl esters are produced in the absence of macrophages. Cumings has, in fact, demonstrated that cholesteryl esters can be found in apparently normal areas of white matter (5, 6), and Greenfield has observed that early demyelination occurs in the absence of any infiltrating cells (7). On the other hand, some authors have postulated that different mech- 725 0364-3190/78/1200-0725505.00/0 ~) 1978Plenum Publishing Corporation