You are here

Cell Rep DOI:10.1016/j.celrep.2019.05.001

Selenium Deficiency Is Associated with Pro-longevity Mechanisms.

Publication TypeJournal Article
Year of Publication2019
AuthorsYim, SHee, Clish, CB, Gladyshev, VN
JournalCell Rep
Volume27
Issue9
Pages2785-2797.e3
Date Published2019 May 28
ISSN2211-1247
Abstract

Selenium (Se) is an essential trace element because of its presence in selenoproteins in the form of selenocysteine residue. Both Se deficiency, which compromises selenoprotein functions, and excess Se, which is toxic, have been associated with altered redox homeostasis and adverse health conditions. Surprisingly, we found that, although Se deficiency led to a drastic decline in selenoprotein expression, mice subjected to this dietary regimen for their entire life had normal lifespans. To understand the molecular mechanisms involved, we performed systemic analyses at the level of metabolome, transcriptome, and microRNA profiling. These analyses revealed that Se deficiency reduced amino acid levels, elevated mononucleotides, altered metabolism, and activated signaling pathways linked to longevity-related nutrient sensing. The data show that the metabolic control associated with nutrient sensing coordinately responds to suppressed selenoprotein functions, resulting in normal lifespan under Se deficiency.

DOI10.1016/j.celrep.2019.05.001
Pubmed

http://www.ncbi.nlm.nih.gov/pubmed/31141699?dopt=Abstract

Alternate JournalCell Rep
PubMed ID31141699