Abstract
Selenium is an essential trace element linked to normal development and antioxidant defense mechanisms through its incorporation into selenoproteins via the amino acid, selenocysteine (Sec). Male mice lacking both the Se transporter, selenoprotein P (SELENOP), and selenocysteine lyase (Scly), which plays a role in intracellular Se utilization, require Se supplementation for viability and exhibit neuromotor deficits. Previously, we demonstrated that male SELENOP/Scly double knockout (DKO) mice suffer from loss of motor function and audiogenic seizures due to neurodegeneration, both of which are alleviated by prepubescent castration. The current study examined the neuromotor function of female DKO mice using the rotarod and open field test, as well as the effects of dietary Se restriction. Female DKO mice exhibited a milder form of neurological impairment than their male counterparts. This impairment is exacerbated by removal of Se supplementation during puberty. These results indicate there is a critical time frame in which Se supplementation is essential for neurodevelopment. These sex-specific differences may unveil new insights into dietary requirements for this essential nutrient in humans.
Highlights
Selenium is an essential micronutrient due to its presence at the catalytic center of selenoenzymes, many of which have been implicated in biological functions that are crucial for human health [1].Selenium is acquired through diet and incorporated into selenoproteins as the amino acid, selenocysteine (Sec)
The results reported show that Se supplementation is crucial in early life for double knockout (DKO) mice of both sexes, and both exhibit neurological deficits even with Se supplementation, but the severity of the phenotype is vastly different in males versus females
We previously reported that MDKOSe mice performed poorly in the rotarod assay at both 8 and
Summary
Selenium is acquired through diet and incorporated into selenoproteins as the amino acid, selenocysteine (Sec). Dietary Se is absorbed in the gut, and enters the liver via the portal vein, wherein it is incorporated into multiple Sec residues in the Se-transporter, Selenoprotein P (SELENOP, formerly SelP or Sepp). Selenoprotein P is secreted from the liver into the plasma, transported to peripheral tissues and taken up in neurons in the brain and Sertoli cells in the testes through apolipoprotein E2 receptor (ApoER2)-mediated endocytosis [2]. Selenocysteine lyase (Scly), expressed in most tissues, but at highest levels in liver, kidney, and testes, followed by the brain, heart, and spleen [4], catalyzes the breakdown of Sec, allowing Se to be recycled for additional selenoprotein synthesis [5].
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