What question did this study set out to answer?

This research aims to investigate the protective effects of sulforaphane against zearalenone-induced toxicity in bovine mammary epithelial cells.

May 27, 2026Open Access

Sulforaphane Alleviates Zearalenone-Induced Oxidative Stress in Bovine Mammary Epithelial Cells

Key Points

This research aims to investigate the protective effects of sulforaphane against zearalenone-induced toxicity in bovine mammary epithelial cells.
MAC-T cells were treated with varying concentrations of zearalenone and sulforaphane for 24 hours.
Cell viability, lactate dehydrogenase release, reactive oxygen species levels, and levels of antioxidant markers were measured.
Gene expression levels of key antioxidant and inflammatory markers were analyzed following treatment.
Treatment with 10 μM zearalenone significantly decreased MAC-T cell viability compared to control.
Sulforaphane treatment at 1, 2.5, and 5 μM improved cell viability and reduced inflammatory markers like IL-6 and TNF-α.
SFN effectively activated the Nrf2 pathway, increasing the expression of antioxidant genes such as HO-1 and GPX1 that were downregulated by ZEA.

Abstract

Zearalenone (ZEA) is a common contaminant in crops and animal feed. However, research on the effects of ZEA on animal mammary tissue is relatively limited. Sulforaphane (SFN) is a naturally active compound mainly derived from cruciferous vegetables (such as broccoli), with significant antioxidant and cytoprotective effects. The purpose of this study is the effect of SFN on ZEA-induced toxicity in bovine mammary epithelial cells (MAC-T). By treating MAC-T cells with different concentrations of ZEA and SFN for 24 h, the results showed that different concentrations of ZEA (10, 20, 40, 60, 80, or 100 μM) could inhibit MAC-T cell viability. Treatment with SFN at concentrations of 1, 2.5, and 5 μM had no significant effect on cell viability. The results of combined treatment with 10 μM ZEA and 1, 2.5, or 5 μM SFN showed that SFN could significantly reverse the decrease in cell viability caused by ZEA; reduce the increase in lactate dehydrogenase (LDH) release, reactive oxygen species (ROS), and malondialdehyde (MDA) content induced by ZEA; and increase the levels of glutathione (GSH), superoxide dismutase (SOD), and mitochondrial membrane potential that were decreased by ZEA. SFN can significantly inhibit the upregulation of interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), and interleukin 1 beta (IL-1β) induced by ZEA exposure and markedly reverse the increase in cell apoptosis rate caused by ZEA. Compared with the control group, the expression of genes nuclear factor erythroid 2–related factor 2 (Nrf2), heme oxygenase 1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), glutamate-cysteine ligase modifier subunit (GCLM), and glutathione peroxidase 1 (GPX1) was significantly reduced in the ZEA group, while the addition of SFN effectively increased the expression levels of these genes. Corresponding protein detection results were consistent with the trends in gene expression. This study demonstrated that SFN alleviates ZEA-induced damage to MAC-T cells by activating the Nrf2 pathway, providing a theoretical basis for the subsequent application of SFN in dairy farming to prevent and control breast health risks related to mycotoxins.

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