Deoxynivalenol (DON) is widely present
in cereals and processed
grains. It can disrupt the blood-testicular barrier (BTB), leading
to sterility in males; however, the mechanism is unknown. In this
study, 30 Kunming mice and TM4 cells were exposed to 0 or 4.8 mg/kg
(28 d) and 0–2.4 μM (24 h) of DON, respectively. Histopathological
findings showed that DON increased BTB permeability in mice, leading
to tight junction (TJ) structural damage. Immunofluorescence results
indicated that DON disrupted the localization of zonula occludens
(ZO)-1. The results of protein and mRNA expression showed that the
expression of ZO-1, occludin, and claudin-11 was reduced, and that
the p38/GSK-3β/snail and p38/ATF-2/MLCK signaling pathways were
activated in mouse testes and TM4 cells. Pretreatment with the p38
inhibitor SB203580 maintained TJ integrity in TM4 cells after exposure
to DON. Thus, DON induced BTB dysfunction in mice by disrupting p38
pathway-mediated TJ expression and distribution.