Evaluating the effect of selenium on spatial memory impairment induced by sleep deprivation

• Published in: Physiology & behavior 2022-02, Vol.244, p.113669-113669, Article 113669
• Main Authors: Massadeh, Adnan M., Alzoubi, Karem H., Milhem, Amal M., Rababa'h, Abeer M., Khabour, Omar F.
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants - pharmacology; Antioxidants - therapeutic use; Hippocampus; Hippocampus - metabolism; Male; Maze Learning; Memory; Memory Disorders - drug therapy; Memory Disorders - etiology; Memory Disorders - prevention & control; Oxidative Stress; Radial Arm Water Maze; Rats; Rats, Wistar; Selenium; Selenium - pharmacology; Sleep deprivation; Sleep Deprivation - complications; Spatial Memory; Superoxide Dismutase - metabolism
• ISSN: 0031-9384; 1873-507X
• DOI: 10.1016/j.physbeh.2021.113669

•Chronic sleep deprivation induced hippocampus-dependent memory impairment.•It also increased oxidative stress levels.•Selenium supplementation prevented these impairments. Sleep deprivation (SD) impairs memory due to disturbing oxidative stress parameters. Selenium is a main component of several antioxidant enzymes and provides a neuroprotective effect. The present study aimed to investigate the potential neuroprotective effect of chronic selenium administration on cognitive impairments induced by chronic SD. Adult male Wister rats were randomly assigned into five groups (n = 12/group). The SD was induced in rats using modified multiple platform model. Selenium (6 µg/kg of animal's body weight) was administered to rats via oral gavage for 6 weeks. The spatial learning and memory were assessed using the radial arm water maze (RAWM). Moreover, we measured the levels of reduced glutathione (GSH), oxidized glutathione (GSSG) and GSH/GSSG, catalase, glutathione peroxidase (GPx), superoxide dismutase (SOD), thiobarbituric acid reactive substances (TBARS) and brain derived neurotrophic factor (BDNF) in the hippocampus. The results indicate that short- and long-term memory were impaired by chronic sleep deprivation (P < 0.05), while selenium administration prevented this effect. Moreover, selenium normalized antioxidants activities which were reduced by SD such as: catalase (P < 0.05), and SOD (P < 0.05), and significantly enhanced the ratio of GSH/GSSG in sleep-deprived rats (P < 0.05), without significant alteration of BDNF (P > 0.05), GSH (P > 0.05), or TBARS levels (P > 0.05). In conclusion, chronic SD induced memory impairment, and chronic treatment with selenium prevented this impairment by normalizing antioxidant enzymes activities in the hippocampus.