Oral administration of lutein attenuates ethanol-induced memory deficit in rats by restoration of acetylcholinesterase activity

The excessive consumption of alcohol affects the central nervous system, resulting in memory and learning deficits. Lutein is a carotenoid known for its antioxidant properties, which can be able to prevent neurodegenerative diseases and cognitive deficits. In the present study, we evaluated the effect of lutein on ethanol-induced memory deficits in the object recognition task in adult rats, as well as the possible involvement of oxidative stress and cholinergic system. Wistar rats were randomly divided into two groups receiving lutein (50 mg/kg) or olive oil (1 mL/kg) by oral gavage once daily for 14 days. On day 8 each group was divided again into two groups receiving either ethanol (3 g/kg) or saline by oral gavage once daily for 7 days. After the last administration, the animals were submitted on the object recognition task 24 h later (on days 15, 16 and 17). After the behavioral test, the hippocampus and cerebral cortex were removed for the determination of oxidative stress indicators (superoxide dismutase, thiobarbituric acid reactive substances, and non-protein thiol) and acetylcholinesterase activity. Ethanol administration induced a memory deficit and increased acetylcholinesterase activity, however, it did not alter the parameters of oxidative stress, evaluated in the cortex and hippocampus. Oral administration of lutein (50 mg/kg during 14 days) attenuated memory deficit and the increase of acetylcholinesterase activity induced by ethanol. These results provide evidence that lutein is an alternative treatment for ethanol-induced memory deficit, and suggest the involvement of cholinergic system.