The authors also observed that in the liver, selenium yeast significantly reduced the abundance of the protein encoded by the Gadd45b gene, demonstrating the protective impact of selenium yeast and contrasting with the inability of inor- ganic and synthesised selenium sources to do so (Figure 3B). Additionally, the authors measured the levels of a marker of oxidative DNA damage (8-oxo-dG) in the liver and found a 27% reduction in 8-oxo-dG in the selenium yeast supple- mented animals, again indicating the protective benefits of selenium yeast (Figure 3C). Perhaps the most surprising additional finding of this study was the marked induction of the p53 gene in the intestinal tissue of animals fed diets containing the chemically synthe- sised selenium source (Figure 4). It is well documented that the tumour suppressor gene p53, a transcription factor that controls cellular response to DNA damage, is induced in the acute cellular response to DNA damage and also in response to chronic, increased damage observed in aging tissues. Therefore, the level of expres- sion of p53 serves as a gauge of the endogenous levels of genomic instability. This suggests that the synthetic selenium source, unlike selenium yeast, promotes intestinal genotox- icity, potentially a reflection of the acute oral toxicity data highlighted in Table 2. In the context of the overall data, it is clear that selenoamino acid and selenoprotein bioavailability will vary between sources as they transit the GI tract. At a more simplistic level, differences in the stability of selenium sources can also be expected to impact parameters such as shelf life and product quality. More importantly, such differences may have a bearing on the toxic potential of different preparations and, in the case of chemically synthesised selenium sources, impart similar toxicity to that of inorganic sodium selenite.
Conclusions • Selenium source differences have implications for product performance ranging from shelf life and toxicology to animal response. • Clear differences in the relative stabilities of selenium prod- ucts can be demonstrated at the product, premix and feed level. • When compared to selenium yeast, chemically synthesised selenomethionine was relatively unstable and had limited cellular potential in terms of promoting an antioxidant re- sponse. • Antioxidant functioning can be compromised after expo- sure to high levels of chemically synthesised selenium. • This can result in altered gene expression patterns leading to oxidative stress and alterations of cellular function, in addi- tion to both cytotoxicity and proteotoxicity.
References upon request ▶ ALL ABOUT FEED | Volume 30, No. 5, 2022 25
Figure 3 – Effect of selenium supplementation on markers of DNA damage. SD: selenium deficient, SM: chemically synthesized Se. SS: sodium selenite, YS: Selenium yeast. Values with different letters indicate statistically significant differences (P<0.05).
A Gadd45b expression Cortex
600 400 200 0
2000 1500 1000 500 0
a b b b
600 400 200 0
Gastrocnemius a
a b b
600 400 200 0
B Liver GADD45B protein a
100 80 60 40 20 0
8 6 4 2 0
SD SM SS YS a a b Intestine a a a b
Liver a a b a
C Liver DNA oxidation
Figure 4 – p53 tumour oncogene expression SD: selenium deficient. SM: chemically synthesized Se. SS: sodium selenite. YS: Selenium yeast.
400 300 200 100 0
SD *
SM
SS *p<0.05 compared to control (SD) levels
YS
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