Cognitive Function and Hippocampal Glutathione and Malondialdehyde Levels in Paraoxon-intoxicated Rats

Exposure to organophosphorus (OP) compounds may contribute to an increased risk of cognitive impairments and induction of oxidative stress. The present study was designed to evaluate the effects of exposure to paraoxon (the active metabolite of insecticide parathion) on cognitive function and oxidative stress biomarkers.

Adult male Wistar rats (n= 56, 7 per group) were used in this study. Corn oil or paraoxon at 0.3, 0.7, or 1 mg/kg were intraperitoneally administrated. After 14 or 28 days, the animals were examined by Morris water maze to determine spatial learning and memory. The effects of paraoxon on hippocampal glutathione (GSH) and malondialdehyde (MDA) levels were also investigated.

Escape latency and swimming distance significantly increased in animals that received 1 mg/kg of paraoxon at both time points (P<0.001 and P<0.05, respectively). In the probe test, animals intoxicated with paraoxon 1 mg/kg spent less time in the target zone and had lower swimming distance and swimming speed compared with the control group. No significant difference was observed in the performance of paraoxon-intoxicated animals in the water maze with visible platform compared with the control group (P>0.05). Exposure to paraoxon 1 mg/kg was associated with decreased GSH and increased MDA levels in the hippocampus.

The study showed that exposure to high dose of paraoxon (1 mg/kg) impaired spatial learning and memory independent of any changes in sensorimotor deficit. Induction of oxidative stress plays an important role in development of cognitive impairments caused by exposure to paraoxon.