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BACKGROUND: The use of nonmammal models in teratological studies is a matter of debate and seems to be justified if the embryotoxic mechanism involves conserved processes. Published data on mammals and Xenopus laevis suggest that azoles are teratogenic by altering the endogenous concentration of retinoic acid (RA). The expression of some genes (Shh, Ptch-1, Gsc, and Msx2) controlled by retinoic acid is downregulated in rat embryos exposed at the phylotypic stage to the triazole triadimefon (FON). In order to propose X. laevis as a model for gene-based comparative teratology, this work evaluates the expression of Shh, Ptch-1, Gsc, and Msx2 in FON-exposed X. laevis embryos. METHODS: Embryos, exposed to a high concentration level (500 µM) of FON from stage 13 till 17, were examined at stages 17, 27, and 47. Stage 17 and 27 embryos were processed to perform quantitative RT-PCR. RESULTS: The developmental rate was never affected by FON at any considered stage. FON-exposed stage 47 larvae showed the typical craniofacial malformations. A significant downregulation of Gsc was observed in FON-exposed stage 17 embryos. Shh, Ptch-1, Msx2 showed a high fluctuation of expression both in control and in FON-exposed samples both at stages 17 and 27. CONCLUSION: The downregulation of Gsc mimics the effects of FON on rat embryos, showing for this gene a common effect of FON in the two vertebrate classes. The high fluctuation observed in the gene expression of the other genes, however, suggests that X. laevis at this stage has limited utility for gene-based comparative teratology. Birth Defects Res (Part B) 92:189–194, 2011. © 2011 Wiley-Liss, Inc.

Summary In order to investigate the relationships between Italian wild boar and major pig breeds, we studied the genetic variability of four wild boar populations in Italy (Arezzo, Pisa, Parma, Bergamo) using a 533-bp fragment of the mitochondrial control region. Sixty-nine wild boar samples were analysed, allowing the identification of 10 distinct haplotypes, which involve a total of 15 single nucleotide polymorphisms. Phylogenetic and network analyses were performed also considering several sequences of wild and domesticated forms available in the databases. The Bayesian phylogenetic tree and the Median-Joining network analyses show three main groups: the Italian (IT), European (EU) and Asian (AS) clades. The IT clade corresponds to the Maremma endemic wild boar population and also includes Sardinian individuals, while the EU and AS groups include wild boars as well as domestic pig breeds. Only two individuals from Pisa cluster in the IT group, whereas two haplotypes from Bergamo cluster in the AS group and all other samples cluster in the EU clade. These findings suggest that in Italy wild boar populations have a mixed origin, both EU and AS, and that an interbreeding between wild and domesticated strains has probably occurred. Eight of the 10 wild boars coming from the Migliarino-San RossoreMassaciuccoli Regional Park (Pisa) belong to H2 and H3 haplotypes, and cluster into the EU clade, suggesting that this regional park is not anymore exclusive of the endemic Maremma wild boar.

BACKGROUND: Since MYS is a microtubular poison with a reversible activity, Xenopus blastulae were exposed to MYS to verify the eventual drug-related developmental suspension and the reversibility of this effect. METHODS: Lethal and teratogenic effects of myoseverin (MYS) were evaluated using the FETAX. Embryos were exposed to different MYS concentrations from stage 8 to stage 47. RESULTS: Probit analysis gave 12.14 µM LC50 and 7.67 µM TC50 from which 1.58 T.I. is derived. Several malformations were observed such as facial abnormalities, abnormal tail flexure, heart ventricle chamber enlargement and external appendix. MYS led to an arrest of living embryo development. Before MYS removing, exposed blastulae showed the lack of mitotic spindles along with different nuclei alterations. Living embryos, moved in control solution, mainly died around the hatching showing severe malformations likely ascribable to the altered planes of newly occurring mitosis. CONCLUSION: In spite of the low T.I, MYS has to be considered a highly teratogenic compound. Birth Defects Res (Part B) 77, 2006. © 2006 Wiley-Liss, Inc.

BACKGROUND: As previously shown, Paraquat (PQ) treatments of Xenopus developing embryos mainly induce a characteristic developmental alteration we named “abnormal tail flexure.” PQ oxidative activity has been indicated as the cause of this malformation. Since PQ evokes reactive oxygen species (ROS), among which hydroxyl radicals (OH•), and H2O2 can be converted to (OH•) via Fenton reaction, we compared here the lethal and teratogenic potentials of both oxidants by using the Frog Embryo Teratogenesis Assay-Xenopus (FETAX), in order to grasp eventual similarities in their teratogenic activity. METHODS:Xenopus embryos were exposed, from stage 8 to stage 47, at 368, 491, 612, and 735 µM H2O2 and 0.388 µM PQ. The probit analysis of H2O2 mortality and malformed larva percents gave a 598.82 µM Lethal Concentration 50% (LC50) and 536.04 µM Teratogenic Concentration 50% (TC50) from which a 1.11 Teratogenic Index (T.I.) has been calculated. This T.I. value should allow the classification of H2O2 as a non-teratogenic compound. RESULTS: A comparison of H2O2 mortality and malformed larva percents with those obtained from PQ exposure showed the higher embryotoxicity of PQ, but, markedly, both compounds mainly induced the “abnormal tail flexure.” Histological analysis of both H2O2 and PQ malformed embryo tails showed a similar distorted morphology of both somites and myocytes. Some of muscle cells were necrotic and affected by an apical enlargement as well as a detachment from the connective tissue of intersomitic boundaries. CONCLUSIONS: In our opinion, both of the tested chemicals likely weaken the mechanical bridge connecting the myocyte contractile apparatus to the extracellular matrix, therefore causing the detachment of some of tail myocytes from their connectival septum as well as their apical enlargement. This could lead to the unbalance of tail tensional forces and, in turn, to the appearance of the “abnormal tail flexure.” Birth Defects Research (Part B) 77:238–243, 2006. © 2006 Wiley-Liss, Inc.