Abstract

ObjectivesSelenium (Se) is both an essential and toxic trace element. In rats and mice, 7 of 25 liver selenoprotein transcripts are significantly downregulated by Se deficiency, but no selenoprotein transcripts are significantly regulated by high Se, and yet 4% of the liver transcriptome is altered by high Se (5 μg Se/g, 50X requirement). Nearly half of regulated genes in Se toxicity are related to the NRF2-mediated response to oxidative stress (Raines & Sunde, BMC Genomics 2011, 12:26). The turkey dietary Se requirement is 4X that of rats or mice (Taylor & Sunde, PLoSone 2017), and previous studies found that no turkey selenoprotein transcript was altered by high Se (Taylor et al., Poult Sci 2018 10.3382/ps/pey413). MethodsTo better understand how turkeys respond to low and high Se status, we characterized the full liver transcriptome in Se-deficient and high-Se vs. Se-adequate turkeys using RNA-seq analysis in poults fed 0.005–5 μg Se/g diet, with adequate dietary vitamin E. ResultsAs in the rodent, we found that the response to Se deficiency was mainly Se-specific — only 13 transcripts were altered by Se deficiency (FDR adjusted P < 0.1), including 6 out of 24 turkey selenoprotein transcripts downregulated to <50% of Se-adequate expression. No turkey selenoprotein transcripts were significantly regulated by high Se, and less than 0.1% of the turkey full transcriptome was altered by high dietary Se (5 μg Se/g, 12.5X requirement). GO analysis implicated no single pathway in response to high Se. ConclusionsThese results indicate that levels of dietary Se, that are toxic in rodents, are not toxic in turkeys; these studies indicate that turkeys adapt to high dietary Se without major changes in transcript expression in liver. Funding SourcesNational Institute of Food and Agriculture USDA Hatch 1,013,496, and by Wisconsin Alumni Foundation 12,046,295.

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