LITHIUM PRESERVES F-ACTIN FROM THE DISARRANGEMENT INDUCED BY EITHER DNASE-I OR CYTOCHALASIN-D

Light scattering at 546 nm, which is mainly related to the presence of rodlike particles longer than 50 nm, showed that Li+ accelerates the formation of actin filaments. Intermolecular cross-linking with N,N-1- 1,4-phenylene-bismaleimide proved that the observed enhancement in the light-scattering intensity is caused by the increase in the concentra tion of actin oligomers, which gradually elongate to form longer filam ents. DNase-I-related F-actin disassembly was reduced in the presence of lithium ions, as demonstrated by fluorimetric and viscometric exper iments. Li+-F-actin showed an apparently similar behaviour when expose d to cytochalasin D. We confirm that Li+ acts on actin polymerization by stabilizing actin nuclei and polymers. The stabilization of cytoske letal polymers really appears as one of the mechanisms by which lithiu m ions influence some of the cell activities.