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

作者：Sehata S^*; Kiyosawa N; Atsumi F; Ito K; Yamoto T; Teranishi M; Uetsuka K; Nakayama H; Doi K

来源：Experimental and Toxicologic Pathology, 2005, 57(1): 15-28.

DOI：10.1016/j.etp.2005.02.005

• T-2 toxin
• pregnant rats
• liver
• placenta
• fetal liver
• apoptosis
• MAPK
• microarray

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 It 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.

• 出版日期2005-8