Exposure to aflatoxin B1 attenuates cell viability and induces endoplasmic reticulum-mediated cell death in a bovine mammary epithelial cell line (MAC-T)

Wonhyoung Park, Min Young Park, Gwonhwa Song, Whasun Lim

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

Mammary gland epithelial cells play a key role in milk production in dairy cattle, which are prone to feed contamination from microorganisms, especially pathogenic fungi and their mycotoxin products. When mycotoxins enter the body, they cause a reduction in feed intake and milk production, leading to the retardation of growth and productivity in dairy cattle. Among them, aflatoxin B1 is a ubiquitous food contaminant frequently found in stored crops, which are used as animal feed, and causes many adverse health effects in domestic animals. Unfortunately, there is a lack of knowledge on the mechanisms underlying the detrimental effects of aflatoxin B1. Therefore, in this study, we found that aflatoxin B1 reduced cellular proliferation, induced apoptosis by DNA fragmentation, and disrupted intracellular homeostasis, including mitochondrial membrane potential and calcium concentration, in an immortalized bovine mammary epithelial cell line (MAC-T). Additionally, we identified aflatoxin B1-mediated cell signaling pathways associated with cell survival and the endoplasmic reticulum stress response. These results revealed that exposure to aflatoxin B1 attenuates cell viability and induces endoplasmic reticulum-mediated cell death in MAC-T cells.

Original languageEnglish
Article number104591
JournalToxicology in Vitro
Volume61
DOIs
Publication statusPublished - 2019 Dec

Keywords

  • Aflatoxin B1
  • Cell death
  • Endoplasmic reticulum stress
  • Mammary gland cell

ASJC Scopus subject areas

  • Toxicology

Fingerprint

Dive into the research topics of 'Exposure to aflatoxin B1 attenuates cell viability and induces endoplasmic reticulum-mediated cell death in a bovine mammary epithelial cell line (MAC-T)'. Together they form a unique fingerprint.

Cite this