Acetylcholinesterase as a potential target of acute neurotoxic effects of lindane in rats

The aim of our study was to investigate the possible involvement of acetylcholinesterase ( AchE) in mediating the early phase of acute lindane neurotoxicityin rats. Male Wistar rats (n = 48) were divided into following groups: 1. control, saline-treated group; 2. dimethylsulfoxide- treated group; 3. group that received lindanedissolved in dimethylsulfoxide, in a dose of 8 mg/kg intraperitoneally. Eight animals from each group were sacrificed 0.5 and 4 h after treatment and brain samples were prepared for further analysis. AchEactivity (mitochondrial and synaptosomalfraction) was determined in cerebral cortex, thalamus, hippocampus and nc. caudatus spectropho- tometrically. A significant increase in mitochondrial AchEactivity was detected in cortex and nc. caudatus of lindane-treated animals 0.5 h after administration ( p < 0.05). This rise was sustained in nc. caudatus within 4 h after treatment ( p < 0.05). In contrast, activity of synaptosomal AchEfraction was significantly increased only in thalamus4 h after lindaneadministration ( p < 0.05). An increase in AchEactivity may be involved in mediating acute neurotoxiceffects of lindane, at least in some brain structures in rats.