Effects of sodium azide on the secretion of soluble amyloid-beta precursorprotein and the accumulation of beta-amyloid (1-40) in cultured chick neurons

Sodium azide has been reported in the literature to reduce the release of s ecreted amyloid beta-precursor protein (A beta PPs) and to produce a large increase in the cellular level of an 11.5 kDa C-terminal A beta PP derivati ve containing the beta-amyloid (AP) sequence. Here we report that 1 mM of s odium azide, reduced the constitutive A beta PPs secretion from cultured em bryonic chick neurons after 12 h of incubation. After 24 h of incubation th ere was a modest increase in lactate dehydrogenase (LDH) release and no cha nge in MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) r eduction, suggesting that the reduced A beta PPs secretion was not due to t he cell toxic effects of NaN3. However, NaN3 reduced the accumulation of A beta(1-40) in the cell lysates and decreased the acetylcholine esterase act ivity both in cell culture media and in cell lysates. It is concluded that the effect of NaN3 upon A beta PP metabolism in the chick cultured neurons may be a rather non-specific effect. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.