ADVERTISEMENT

Home| Journals| Articles by Year| Audio Abstracts
 

Research Article

Open Vet J. 2026; 16(8): 5479-5485


Zearalenone drives apoptosis and oxidative damage in bovine mammary epithelial cells

Xinyu Chen, Qi Kong, Haixu Xu, Nannan Zhao.



Abstract
Download PDF Post

Background:
Zearalenone (ZEA) is a mycotoxin produced by Fusarium fungi that is widely present in animal and human food.

Aim:
This study aimed to systematically evaluate the toxicological effects of ZEA on bovine mammary epithelial cells (MAC-T).

Methods:
To assess cell viability and apoptosis, MAC-T cells were exposed to various concentrations of ZEA for 24 hours, and the optimal ZEA dose was determined for subsequent experiments.

Results:
A dose-dependent decrease in cell viability and a simultaneous increase in apoptotic proportion were observed by flow cytometry. Western blot analysis revealed that ZEA markedly decreased the level of the antiapoptotic protein Bcl-2 and increased the level of the proapoptotic protein Bax. Cellular reactive oxygen species (ROS) and malondialdehyde concentrations were significantly increased, while glutathione peroxidase (GSH-Px) activity and mitochondrial membrane potential were notably reduced. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that ZEA exposure disrupted endoplasmic reticulum function, amino acid metabolism, and glutathione metabolism, among other pathways.

Conclusion:
ZEA induces apoptosis in MAC-T cells by disrupting mitochondrial dysfunction, increasing ROS production, and triggering oxidative stress. These findings offer experimental evidence that may inform strategies for mitigating ZEA-induced milk production losses and mammary health issues in dairy farming.

Key words: Zearalenone; Bovine mammary epithelial cells; Apoptosis; Oxidative damage.







Bibliomed Article Statistics

22
R
E
A
D
S

6
D
O
W
N
L
O
A
D
S
08
2026

Full-text options


Share this Article


Online Article Submission
• ejmanager.com




ejPort - eJManager.com
Author Tools
About BiblioMed
License Information
Terms & Conditions
Privacy Policy
Contact Us

The articles in Bibliomed are open access articles licensed under Creative Commons Attribution 4.0 International License (CC BY), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.