Selenium concentration in the brain tissue is far less variable than those in peripherals, such as the liver and kidneys, in rodents, when fed a selenium-deficient diet. This fact implies the importance of this element for maintaining the integrity of brain functions and the distinctive selenium metabolism and/or the regulatory mechanism in the brain. To obtain basic information concerning the homeostatically maintained selenium store in the brain, we investigated absorption and retention characteristics of selenium from selenious acid (SA) and seleno-L-methionine (SeMet) in rat dorsal root ganglion (DRG) neurons, in comparison to isolated rat hepatocytes and renal cellsin vitro. When DRG neurons were cultured in an SA-free medium subsequent to an SA-supplemented one for 24 h, the DRG neurons maintained a higher selenium concentration than that before SA supplementation over a period of 96 h after removal of SA from the culture medium. The cellular glutathione peroxidase activity of the cells increased for 72 h after removal of SA from the culture medium. A similar retention characteristic of selenium was also observed for DRG neurons treated with SeMet-supplemented culture medium. Consequently, selenium from source compounds, in part, was thought to be retained in DRG neurons and then be utilized for the synthesis of selenium-containing proteins, which implied the presence of a neuron-specific selenium retention mechanism.
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