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Dimethoate (DMT), a widely used Organophosphorous insecticide, was administered for 5weeks (sub-chronic) at low dose (15mg/kg b.w.) to male Wistar rats with the aim to simulate potential exposure to pesticide residues in food and water. The induction of cell death programs was investigated in two brain regions, cortex (Cx) and substantia nigra (SN), after the exposure period. We found that DMT increased cytochrome C (CytC) release from mitochondria, the Bax/Bcl-2 ratio, the activity of caspase-3 and calpains, in both brain regions compared to VEH injected ones. DMT treatment induced oxidative damage of lipids with a consequent enrichment in saturated over unsaturated fatty acids. However, the activity of mitochondrial respiratory complexes was not affected by DMT treatment. The activation of the pro-apoptotic pathway can be correlated with a decrease of TH-immunoreactive neurons in SN, comparable to the reduction observed in this cell population by aging. The results of this work contribute to understand the toxic mechanism of DMT and the possible etiological role that residues of this insecticide, might play in neurodegenerative diseases.In rats, the exposure to low doses of DMT for a sub-chronic period induce the activation of cell death programs in brain.The oxidation of polyunsaturated fatty acids from the mitochondrial membrane leads to the activation of cell death programs.The activation of the pro-apoptotic pathway is associated with a reduction of TH-immunoreactive neurons.The effect of the sub-chronic exposure to DMT can be comparable to the effect of normal ageing.