The aim of this study was to investigate the dynamics of lipid peroxidation and the possible correlation between lipid peroxidation in different brain regions and behavioral manifestations in
lindane-induced
seizures in rats. Male Wistar rats were divided into the following groups: 1. control, saline-treated group; 2.
dimethylsulfoxide (
DMSO)-treated group; 3.
lindane-treated group (8 mg/kg), intraperitoneally. Animals were sacrificed 0.5 or 4 h
after treatment and the
malondialdehyde level and
superoxide dismutase (SOD) activity were determined in various brain regions spectrophotometrically. Behavioral changes were classified according to the descriptive scale (0--no response, 1--head nodding, lower jaw twitching; 2--myoclonic body jerks, bilateral forelimb clonus with full rearing; 3--progression to generalized clonic convulsions followed by tonic extension of fore- and hind limbs and tail; 4--
status epilepticus). A significant rise in the
malondialdehyde level was detected in the cerebral cortex, hippocampus, and thalamus of
lindane-treated animals 0.5 and 4 h after administration (P < 0.05). SOD activity (total and mitochondrial) was significantly decreased in the hippocampus and the cortex of
lindane-treated animals at both time points (P < 0.05). An initial fall in SOD activity was detected in the thalamus 4 h after
lindane administration (P < 0.05). A positive correlation between seizure severity and the
malondialdehyde level was found in the hippocampus at both time points (P < 0.01). These results suggest that lipid peroxidation may contribute to the neurotoxic effects of
lindane in early acute
lindane intoxication and that behavioral manifestations correlate with lipid peroxidation in the hippocampus of
lindane-treated rats.