Fish Oil Ameliorates Deoxynivalenol-Induced Liver Injury Through Modulating Ferroptosis Signaling Pathway in Weaned...

Area of Science:

• Veterinary Medicine
• Toxicology
• Biochemistry

Background:

• Deoxynivalenol (DON) is a mycotoxin causing significant liver injury in livestock.
• Hepatic diseases are a growing concern in animal agriculture.
• Ferroptosis, a regulated cell death pathway, is implicated in liver damage.

Purpose of the Study:

• To investigate the protective effects of dietary fish oil (FO) against DON-induced liver injury in weaned piglets.
• To determine if FO modulates the ferroptosis signaling pathway in the context of DON exposure.
• To evaluate the impact of FO on oxidative stress markers and hepatic structural integrity.

Main Methods:

• A 2x2 factorial design study with 24 weaned piglets.
• Treatments included dietary corn oil vs. 5% fish oil and basal diet vs. 4 mg/kg DON contamination.
• Analysis of liver and serum samples for biochemical markers, oxidative stress indicators, gene expression, and protein levels related to ferroptosis.

Main Results:

• Fish oil (FO) supplementation significantly reduced DON-induced hepatic damage, inflammation, and elevated liver enzymes (AST, ALP).
• FO decreased markers of lipid peroxidation (MDA, 4-HNE) and iron overload (Fe2+), while increasing antioxidant capacity (GSH).
• FO modulated key genes and proteins in the ferroptosis pathway, including SLC7A11, TFR1, FTH, and GPX4, counteracting DON-induced alterations.

Conclusions:

• Dietary fish oil (FO) ameliorates deoxynivalenol (DON)-induced liver injury in weaned piglets.
• FO's protective effects are likely mediated by suppressing the ferroptosis signaling pathway and reducing oxidative stress.
• FO supplementation represents a promising nutritional strategy to mitigate mycotoxin-induced liver damage in swine.