Neuronal Apoptosis and Imbalance of Neurotransmitters Induced by Acetamiprid in Rats

International audience

English. Recent toxicological studies have demonstrated that exposure to organochlorine pesticides is susceptible to produce various alterations in brain cell which significantly contribute to a loss in neurobehavioral skills and disturbance of neuronal function. Acetamipride (AC) is belonging to this organochlorines family and it is considered less harmful by toxicovigilance systems and practices in Algeria. The aim of this work was mainly to evaluate the impact of this pesticide on the brain cell integrity and function in Acetamiprid-treated rats at the dose of 3.14 mg/kg (1/60 Lethal Dose) daily during 3 months. Several indicators of neuronal apoptosis and function have been rated, in addition to classical labyrinth and Maze tests monitoring to evaluate learning and memorization abilities in rats exposed to this neonicotinoid. The results of this study have shown significant enhancing of cytochrome-c (p <= 0.01) and Caspase-3 (p<0.001) activities in brain lysates of treated group that is correlated with induction of apoptosis. At the same time, assessment of neurotransmitters brain cells has recorded a significant in-crease (p <= 0.01) in adrenaline rate and a significant decrease in cerebral level of dopamine (p <= 0.01), serotonin (p <= 0.001) and Acetylcholin esterase in the same group comparing to control. Furthermore, neurobehavioral study has shown a strong correlation between the unbalance observed in neurotransmitters homeostasis and the significant (p <= 0.01) loss of learning, memorization and locomotive potential as demonstrated by the increase in arrival time (S) (10.33 +/- 3.14) versus (3.33 +/- 2.05) in control. In conclusion, exposition of the rats to Acetamiprid generates apoptosis which is induced by releasing of mitochondrial Cytochrome-c in cell cytosol and alters neurotransmitters rates that could reduce the potential of learning and memorization in the rats.