Possible role of sertraline against 3-nitropropionic acid induced behavioral, oxidative stress and mitochondrial dysfunctions in rat brain.

Oxidative stress and disrupted energy metabolism are major events leading to nerve cell death. Oxidative stress and related reactive oxygen species is one of the common cooperative sharing pathways involved in neurodegenerative disorders including Huntington's disease. The present study evaluated the possible role of sertraline on the 3-nitropropionic acid induced behavioral, biochemical, and mitochondrial alterations in discrete areas of rat brain. 3-Nitropropionic acid (10 mg/kg) administration for 14 days significantly induced Huntington's disease like symptoms in rats as indicated by change in locomotor activity, body weight, rotarod activity performance, oxidative damage (elevated levels of lipid peroxidation, nitrite concentration, depletion of antioxidant enzyme levels) and mitochondrial dysfunction (Complexes-I, II, II and IV) in striatum, cortex and hippocampal region of brain. Treatment with sertraline (5 and 10 mg/kg) significantly reversed behavioral, biochemical and mitochondrial enzyme dysfunctions in 3-nitropropionic acid treated group. Further, combination of yohimbine (2 mg/kg) (non selective serotonin with the higher dose of sertraline (10 mg/kg) did not influence the protective action of sertraline. The present study suggests the possible antioxidant role of sertraline against 3-nitropropionic acid induced alterations in animals.