Abstract:
:Azole derivatives are teratogenic in rats and mice in vitro and in vivo. The postulated mechanism for the dysmorphogenetic effects is the inhibition of retinoic acid (RA)-degrading enzyme CYP26. Azole-related abnormalities are confined to structures controlled by RA, especially the neural crest cells, hindbrain, cranial nerves, and craniofacial structures, through a complex signal cascade. The aim of this work is to study the expression of signal molecules activated by RA (TGF-betas) or involved in the modulation of cellular RA concentrations (CRABPI). E9.5 (9.5 day post coitum old embryos) rat embryos, exposed in vitro to triadimefon (FON) for 24 h, were examined or cultured in normal serum for extra 4, 16, and 24 h. RT-PCR was performed to quantify TGF-beta1, TGF-beta2, TGF-beta3, TGF-betaRI, TGF-betaRII, and TGF-betaRIII mRNA in the hindbrain after 24 h of culture. TGF-beta1, TGF-beta2, and TGF-betaRI were found significantly decreased by FON exposure, and consequently their protein expression was analyzed by Western blot and immunohistochemistry. In both controls and FON-exposed embryos, TGF-beta1 and TGF-betaRI were detected at 24 and 24+4 h; TGF-beta2 was present only at 24 h. Only TGF-beta1 was expressed at the level of hindbrain and branchial tissues. After quantization, TGF-beta1 was reduced in the FON group. The expression of CRABPI was observed at all developmental stages. However, in FON-exposed embryos, it was increased at 24 and 24+4 h. The hindbrain distribution of CRABPI-positive cells was abnormal in FON-exposed embryos. The results show that the two RA-related molecules (TGF-beta1 and CRABPI) are altered by FON exposure in vitro.
journal_name
Toxicol Appl Pharmacoljournal_title
Toxicology and applied pharmacologyauthors
Di Renzo F,Corsini E,Broccia ML,Marinovich M,Galli CL,Giavini E,Menegola Edoi
10.1016/j.taap.2008.09.025subject
Has Abstractpub_date
2009-01-01 00:00:00pages
107-16issue
1eissn
0041-008Xissn
1096-0333pii
S0041-008X(08)00415-8journal_volume
234pub_type
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