Microarray analysis of T-2 toxin-induced liver, placenta and fetal liver lesions in pregnant rats

Exp Toxicol Pathol. 2005 Aug;57(1):15-28. doi: 10.1016/j.etp.2005.02.005.


Pregnant rats on day 13 of gestation were treated orally with 2 mg/kg of T-2 toxin and sacrificed at 1, 3, 6, 9 and 12 h after the treatment (HAT). Histopathologically, the number of apoptotic cells was increased in the liver, placenta and fetal liver (peaked at 6, 12 and 9-12 HAT, respectively). To examine the gene expression profiles, we performed microarray analysis of these tissues at two selected time points based on the results of the TdT-mediated dUTP nick end labeling (TUNEL) staining. Increased expression of oxidative stress- and apoptosis-related genes was detected in the liver of dams, placenta and fetal liver of pregnant rats treated with T-2 toxin at the peak time point of apoptosis. Decreased expression of lipid metabolism- and drug-metabolizing enzyme-related genes was also detected in these tissues. The results suggested that the mitogen-activated protein kinase (MAPK) pathway might be involved in the mechanism of T-2 toxin-induced apoptosis. In addition, increased expression of the c-jun gene was consistently observed in these tissues. Our results suggest that the mechanism of T-2 toxin-induced toxicity in pregnant rats is due to oxidative stress followed by the activation of the MAPK pathway, finally inducing apoptosis. The c-jun gene may play an important role in T-2 toxin-induced apoptosis.

MeSH terms

  • Administration, Oral
  • Animals
  • Apoptosis / drug effects
  • Female
  • Fetus / drug effects*
  • Fetus / metabolism
  • Fetus / pathology
  • Gene Expression Profiling*
  • Gene Expression Regulation, Developmental / drug effects*
  • Genes, jun
  • In Situ Nick-End Labeling
  • Liver / drug effects*
  • Liver / embryology
  • Liver / metabolism
  • Liver / pathology
  • Maternal Exposure
  • Mitogen-Activated Protein Kinases / drug effects
  • Mitogen-Activated Protein Kinases / genetics
  • Oxidative Stress
  • Placenta / drug effects*
  • Placenta / metabolism
  • Placenta / pathology
  • Pregnancy
  • Protein Array Analysis
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Reverse Transcriptase Polymerase Chain Reaction
  • T-2 Toxin / toxicity*


  • RNA, Messenger
  • Mitogen-Activated Protein Kinases
  • T-2 Toxin