# Plasma Metabolomics Reveals Systemic Metabolic Remodeling in Early-Lactation Dairy Cows Fed a Fusarium-Contaminated Diet and Supplemented with a Mycotoxin-Deactivating Product

**Authors:** Gabriele Rocchetti, Alessandro Catellani, Marco Lapris, Nicole Reisinger, Johannes Faas, Ignacio Artavia, Silvia Labudova, Erminio Trevisi, Antonio Gallo

PMC · DOI: 10.3390/toxins18010009 · Toxins · 2025-12-22

## TL;DR

This study shows how a mycotoxin-deactivating product can reduce harmful metabolic changes in cows fed a Fusarium-contaminated diet.

## Contribution

The study introduces a mycotoxin-deactivating product that mitigates metabolic stress in cows exposed to Fusarium toxins.

## Key findings

- Mycotoxin exposure altered sphingolipid metabolism and caused oxidative DNA damage in cows.
- MDP supplementation reduced sphingolipid intermediates and oxidative stress markers.
- MDP improved mitochondrial function and redox homeostasis, as suggested by metabolite changes.

## Abstract

This study investigated the systemic metabolic effects of feeding a Fusarium-contaminated diet to early-lactation Holstein cows, with or without a mycotoxin-deactivating product (MDP; Mycofix® Plus, BIOMIN Holding GmbH, Tulln, Austria). Thirty cows were divided into three dietary groups: a mildly contaminated control (CTR), a moderately contaminated diet containing zearalenone and deoxynivalenol (MTX), and the same contaminated diet supplemented with MDP. Plasma collected at 56 days in milk was analyzed by untargeted ultra-high-performance liquid chromatography (UHPLC) coupled with high-resolution mass spectrometry (HRMS), and multivariate models identified discriminant metabolites and pathways. MTX-fed cows showed alterations in sphingolipid metabolism, including accumulation of ceramide (t18:0/16:0), lactosylceramide, and sphinganine 1-phosphate, consistent with ceramide synthase inhibition and lipid remodeling stress. Increases in estradiol, estrone, and cholesterol sulfate suggested endocrine disruption, while elevated 8-oxo-dGMP indicated oxidative DNA damage. MDP supplementation mitigated these alterations, reducing sphingolipid intermediates, modulating tryptophan and glycerophospholipid pathways, and lowering oxidative stress markers. Metabolites such as riboflavin, pipecolic acid, and N-acetylserotonin could be likely associated with an improved mitochondrial function and redox homeostasis, although future studies are required to confirm this hypothesis. Additionally, MDP-fed cows exhibited distinct shifts in pyrimidine and nucleotide metabolism. Overall, MDP effectively counteracted Fusarium-related metabolic disturbances, supporting its protective role in maintaining lipid balance, hormonal stability, oxidative control, and metabolic resilience.

## Linked entities

- **Chemicals:** zearalenone (PubChem CID 5281576), deoxynivalenol (PubChem CID 40024), ceramide (PubChem CID 139583739), lactosylceramide (PubChem CID 6450208), sphinganine 1-phosphate (PubChem CID 644260), estradiol (PubChem CID 450), estrone (PubChem CID 5870), cholesterol sulfate (PubChem CID 65076), 8-oxo-dGMP (PubChem CID 135488904), riboflavin (PubChem CID 1072), pipecolic acid (PubChem CID 849), N-acetylserotonin (PubChem CID 903)

## Full-text entities

- **Diseases:** endocrine disruption (MESH:D004700)
- **Chemicals:** MTX (-), estradiol (MESH:D004958), sphingolipid (MESH:D013107), ceramide (MESH:D002518), pipecolic acid (MESH:C031345), lipid (MESH:D008055), lactosylceramide (MESH:C009744), cholesterol sulfate (MESH:C007045), riboflavin (MESH:D012256), tryptophan (MESH:D014364), sphinganine 1-phosphate (MESH:C060504), glycerophospholipid (MESH:D020404), estrone (MESH:D004970), N-acetylserotonin (MESH:C006389), deoxynivalenol (MESH:C007262), 8-oxo-dGMP (MESH:C515742), zearalenone (MESH:D015025)
- **Species:** Bos taurus (bovine, species) [taxon 9913]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12846448/full.md

## References

44 references — full list in the complete paper: https://tomesphere.com/paper/PMC12846448/full.md

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Source: https://tomesphere.com/paper/PMC12846448