# Proteomic Analysis Reveals the Protective Effects of Selenomethionine Against Liver Oxidative Injury in Piglets

**Authors:** Kai Zhang, Shuhui Yan, Junhong Miao, Wen Li, Zhenxu Li

PMC · DOI: 10.3390/ani15131989 · Animals : an Open Access Journal from MDPI · 2025-07-07

## TL;DR

This study shows that adding selenomethionine to piglet diets protects their livers from oxidative stress and improves growth.

## Contribution

The study reveals new insights into how selenomethionine protects piglet livers through selenoprotein upregulation and fatty acid metabolism.

## Key findings

- SeMet supplementation improved growth and liver health in piglets under oxidative stress.
- SeMet increased antioxidant enzyme activity and reduced oxidative damage markers.
- Proteomic analysis linked SeMet's benefits to fatty acid metabolism and selenoprotein gene upregulation.

## Abstract

Oxidative stress is recognized as a significant challenge in pig production, particularly during the piglet stage. The liver, as the central organ, is particularly susceptible to oxidative stress. Selenium is an essential trace element for human and animal health, primarily involved in the antioxidant system through selenoproteins. Supernutritional selenium supplementation has been shown to provide various beneficial effects, including antioxidant and anti-stress functions. Therefore, in this study, we aimed to investigate the protective effects and mechanisms of supernutritional selenomethionine (SeMet) supplementation against oxidative liver injury in piglets. Our results indicated that SeMet supplementation improved growth performance and liver health in piglets exposed to oxidative stress. The beneficial effects of SeMet may be correlated with the upregulation of certain selenoprotein mRNA levels (e.g., GPX1/3, DIO2, and SELENOF/M/W). Furthermore, proteomic analysis indicated that the fatty acid metabolism signaling pathway may play a crucial role in the alleviation of liver oxidative damage in piglets by SeMet.

This study investigated the protective effects of high selenomethionine (SeMet) supplementation on liver injury caused by oxidative stress in piglets and explored the underlying mechanisms. A total of 18 piglets were randomly assigned to three groups, with six replicates in each group. The control (CON) and diquat (DQ) groups were fed a basal diet supplemented with 0.3 mg Se/kg Se, while the SeMet group received a basal diet supplemented with 1.0 mg Se/kg. The results indicated that SeMet supplementation significantly improved growth performance and increased the serum and liver activities of antioxidant enzymes. Additionally, it reduced the serum and liver levels of malondialdehyde and protein carbonyls in piglets exposed to DQ. Selenoprotein transcriptome analysis showed that the mRNA levels of five selenoprotein genes (GPX1/3, DIO2, and SELENOF/M/W) were significantly upregulated by dietary SeMet supplementation in the liver of DQ-challenged piglets. Proteomic analysis revealed that a total of 3614 proteins were identified in the liver of piglets. Among them, 85 differentially expressed proteins (DEPs) were identified between the CON and DQ groups, 58 DEPs were observed between the DQ and SeMet groups, and 113 DEPs were identified between the CON and SeMet groups. KEGG analysis indicated that most of the DEPs observed among the three groups were involved in fatty acid metabolism, glycolysis/gluconeogenesis, and the PPAR signaling pathway. Together, these results indicate that dietary supplementation with supernutritional SeMet alleviates the negative effects of the DQ challenge on growth performance and liver injury in piglets. This effect is associated with increased antioxidant capacity, enhanced expression of certain selenoprotein genes, and the regulation of fatty acid metabolism.

## Linked entities

- **Genes:** GPX1 (glutathione peroxidase 1) [NCBI Gene 2876], GPX3 (glutathione peroxidase 3) [NCBI Gene 2878], DIO2 (iodothyronine deiodinase 2) [NCBI Gene 1734], SELENOF (selenoprotein F) [NCBI Gene 9403], SELENOW (selenoprotein W) [NCBI Gene 6415]
- **Chemicals:** selenomethionine (PubChem CID 15103), SeMet (PubChem CID 105024), diquat (PubChem CID 6795), malondialdehyde (PubChem CID 10964)
- **Species:** Sus scrofa (taxon 9823)

## Full-text entities

- **Genes:** DIO2 (iodothyronine deiodinase 2) [NCBI Gene 1734] {aka 5DII, D2, DIOII, SELENOY, SelY, TXDI2}, SELENOF (selenoprotein F) [NCBI Gene 9403] {aka SEP15}, PPARA (peroxisome proliferator activated receptor alpha) [NCBI Gene 5465] {aka NR1C1, PPAR, PPAR-alpha, PPARalpha, hPPAR}
- **Diseases:** liver injury (MESH:D017093), Liver Oxidative Injury (MESH:D008107)
- **Chemicals:** malondialdehyde (MESH:D008315), fatty acid (MESH:D005227), DQ (MESH:D004178), Se (MESH:D012643), SeMet (MESH:D012645)

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12248808/full.md

## References

47 references — full list in the complete paper: https://tomesphere.com/paper/PMC12248808/full.md

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Source: https://tomesphere.com/paper/PMC12248808