All rights reserved.”
“Inhalation of particles has been shown to induce mutations in the male germline in mice following both prenatal and adult exposures in several experiments. In contrast, the effects of particles on female germ cell mutagenesis are not well established. Germline mutations are induced during active cell division, which occurs during fetal development in females. We investigated the effects of prenatal

exposure to carbon black nanoparticles (CB) on induction of mutations in the female mouse germline during this website fetal development, spanning the critical developmental stages of oogenesis. Pregnant C57BL/6J mice were exposed four times during gestation by intratracheal instillation of 67 mu g/animal of nanosized carbon black Printex90 or vehicle (gestation days 7, 10, 15 and 18). Female offspring were raised to maturity and mated with unexposed CBA males. Expanded simple tandem repeat (ESTR) germline mutation rates in the resulting F2 generation were determined from full pedigrees (mother, father, offspring) of F1 female mice (178 CB-exposed and 258 control F2 offspring). ESTR mutation rates in CB-exposed

F2 female offspring were Crenolanib research buy not statistically different from those of F2 female control offspring. (C) 2013 Elsevier Inc. All rights reserved.”
“The eye is particularly sensitive to ethanol’s teratogenic effects. Our previous work, using a chick embryo model system, has shown that ethanol acts rapidly to perturb vital processes of early eye development producing defects of the lens and retina. Ethanol-induced selleck kinase inhibitor disruption of the midline ventral telencephalon, a key site for expression of ocular morphogens such as sonic hedgehog (Shh), was further established. Consequently, in this study we have examined the effects of ethanol on the Shh pathway during the period of optic

vesicle/optic cup formation. Chick embryos were injected in ovo with 125 mu L of a 20% ethanol solution directly into the yolk-sac at HH-stage 7, resulting in peak ethanol uptake of 0.294 g/dL. Subsequent molecular analysis at 12, 24 and 48 h post-treatment revealed that ethanol had no affect on Shh transcription, while, a significant reduction in the expression of the active signalling Shh protein was found. Surprisingly, none of the downstream Shh pathway members (Ptc, Gli1 and Gli3) were significantly altered by ethanol exposure. Overall, our results indicate that ethanol’s disruption of Shh may be mediated through some alternative mechanism independent of the classical signalling pathway. However, the precise role of Shh in relation to ethanol teratogenicity continues to be debated. Thus, in conclusion, our findings are discussed in relation to the varied and often conflicting reports of ethanol-induced Shh perturbation found in the literature. (C) 2013 Elsevier Inc. All rights reserved.”
“Transcriptomic evaluations may improve toxicity prediction of in vitro-based developmental models.