Effect of lycopene and epigallocatechin-3-gallate against 3-nitropropionic acid induced cognitive dysfunction and glutathione depletion in rat: a novel nitric oxide mechanism.

Huntington's disease is a neurodegenerative disorder characterized by symptoms like chorea and dementia. There is no exact therapeutic agent available to manage and cure this disease. 3-Nitropropionic acid, a neurotoxin causes gait and memory impairment which leads to oxidative damage and upsets glutathione defense in animals. 3-NP model is a useful tool to develop suitable therapeutic agent in the treatment of Huntington's disease. Present study compares the effects of lycopene and epigallocatechin-3-gallate (EGCG) on memory impairment and disturbs glutathione system against 3-NP treatment. 3-NP treatment significantly impaired memory as assessed in Morris water maze and elevated plus maze tasks. On the 15 day, the levels of reduced glutathione, total glutathione and glutathione-S-transferase were also significantly decreased in the striatum, hippocampus and cortex areas of the brain. The treatment with lycopene (2.5, 5 and 10mg/kg) and EGCG (10, 20 and 40 mg/kg) significantly improved memory and restored glutathione system functioning. Further, L-arginine and L-NAME pretreatment with the sub effective dose of lycopene (5mg/kg) and EGCG (20mg/kg) reversed and potentiate their protective effects respectively. In conclusion, lycopene and EGCG could be used to mange 3-NP induced behavioral and biochemical alterations by involving nitric oxide pathways.