Juvenile Selenium Deficiency Impairs Cognition, Sensorimotor Gating, and Energy Homeostasis in Mice.

Victor W Kilonzo,Jennifer M Pilat,Alexandru R Sasuclark,Christopher S Williams,Celine Coyle,Matthew W Pitts,Daniel J Torres

doi:10.3389/fnut.2021.667587

Abstract

Selenium (Se) is an essential micronutrient of critical importance to mammalian life. Its biological effects are primarily mediated via co-translational incorporation into selenoproteins, as the unique amino acid, selenocysteine. These proteins play fundamental roles in redox signaling and includes the glutathione peroxidases and thioredoxin reductases. Environmental distribution of Se varies considerably worldwide, with concomitant effects on Se status in humans and animals. Dietary Se intake within a narrow range optimizes the activity of Se-dependent antioxidant enzymes, whereas both Se-deficiency and Se-excess can adversely impact health. Se-deficiency affects a significant proportion of the world's population, with hypothyroidism, cardiomyopathy, reduced immunity, and impaired cognition being common symptoms. Although relatively less prevalent, Se-excess can also have detrimental consequences and has been implicated in promoting both metabolic and neurodegenerative disease in humans. Herein, we sought to comprehensively assess the developmental effects of both Se-deficiency and Se-excess on a battery of neurobehavioral and metabolic tests in mice. Se-deficiency elicited deficits in cognition, altered sensorimotor gating, and increased adiposity, while Se-excess was surprisingly beneficial.

Highlights

Selenium (Se) is an essential trace element in mammals, of which both deficiency and excess can have detrimental effects on health [1]
Newly weaned male mice were allocated into three groups devised to represent conditions of Se-deficiency (Se-def), Se-supplementation (Se-sup), and Se-excess (Se-exc)
We probed for GPX1 and TXNRD2, two abundant selenoproteins known to be responsive and non-responsive to alterations in Se supply [28], respectively, and the selenium binding protein (SELENBP1), a putative factor protecting against Se-toxicity [29]

Summary

Introduction

Selenium (Se) is an essential trace element in mammals, of which both deficiency and excess can have detrimental effects on health [1]. Se supplementation within a narrow range optimizes activity of Se-dependent antioxidant enzymes that incorporate Se co-translationally in the form of selenocysteine. Deficient Se intake impairs thyroid hormone metabolism and reduces activity of the antioxidant enzymes, glutathione peroxidase and thioredoxin reductase [4]. Se-deficiency is estimated to occur in roughly 10% of the world’s population and is observed predominantly in regions with low soil Se-content, such as Scandinavia, New Zealand, and Northeast China [6]. Future climate change is predicted to decrease soil Se content in agricultural regions and augment the prevalence of Se-deficiency worldwide [7]. Common symptoms associated with Se-deficiency include hypothyroidism, cardiomyopathy, compromised

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Conclusion