Drug Toxicity in Embryonic Development II: Advances in by D. M. Kochhar (auth.), Robert J. Kavlock Ph.D., George P.

By D. M. Kochhar (auth.), Robert J. Kavlock Ph.D., George P. Daston Ph.D. (eds.)

Having acquired the invitation from Springer-Verlag to supply a quantity on drug-induced start defects for the instruction manual of Experimental Pharmacology, we requested ourselves what new strategy might we provide that might seize the country of the technological know-how and convey a brand new synthesis of the data in this subject to the world's literature. We selected a three-pronged procedure, headquartered round these specific medicinal drugs for which we now have a comparatively good proven foundation for figuring out how they exert their negative effects at the human embryo. We then supplemented this knowledge with a sequence of studies of serious organic strategies occupied with the confirmed general developmental styles, with emphasis on what occurs to the embryo whilst the approaches are perturbed by means of experimental potential. figuring out that the hunt for mechanisms in teratology has usually been inhibited via the shortcoming of realizing of ways general improvement proceeds, we additionally integrated chapters describing the superb new discoveries concerning the molecular regulate of ordinary morphogenesis for a number of organ platforms within the desire that experimental toxicologists and molecular biologists will start to higher get pleasure from every one others questions and development. a number of instances over the past years of constructing outlines, issuing invites, reviewing chapters, and cajoling belated individuals, we now have questioned no matter if we made the right kind determination to adopt this effort.

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Extra resources for Drug Toxicity in Embryonic Development II: Advances in Understanding Mechanisms of Birth Defects: Mechanistic Understanding of Human Developmental Toxicants

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1994). Since all-trans RA is considerably more potent than 13-cis RA in eliciting a teratogenic response in ICR mice, we compared the time course of induction of RAR~2 mRNA after a single dose of 100 mg all-trans RA/kg and three doses of 100 mg 13-cis RA/kg given 3 h apart. RAR~2 mRNA levels in the treated Retinoids 25 embryos were elevated by either isomer to manyfold higher than the levels in the tissues of the control, untreated embryos. In the limb buds, both isomers raised RAR~2 mRNA levels about 14-fold higher than the basal level.

Exposure occurring on GD 12-14 often is associated with limb and genitourinary defects. 2. The teratogenic response is dose dependent. Higher doses not only increase the frequency and severity of defects, they also cause embryolethality. One needs relatively low doses during early phases and higher doses during later phases of organogenesis for the teratogenic response. During the critical developmental stage of a given organ, the teratogenic response is proportional to the amount of all-trans RA localized in the embryo.

1990). Again, RARy null mutants showed early postnatal mortality and male sterility, but harbored only a few minor congenital defects, which were much milder than what would be expected from the spatiotemporal distribution of this receptor in the embryo (LOHNES et al. 1993). For instance, no limb malformations occurred even though RARy is known to be uniformly expressed during early morphogenesis and thereafter becoming restricted to precartilage condensations (DOLLE et al. 1989b; RUBERTE et al.

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