Teratogenesis structure

Adams J (1993) Structure-activity and dose-response relationships in the neural and behavioral teratogenesis of retinoids. Neurotoxicol Teratol, 15(3) 193-202. 

DNA repair is deficient are more susceptible to these reactions (115). Therefore, although the exact changes in macromolecular structure and function responsible for phenytoin teratogenesis remain to be identified, it is likely that DNA damage plays a critical role in much the same way as has been described for carcinogenic reactions. 

Vijay KG, Borgstedt H, Enslein K et al. A QSAR Model of Teratogenesis. Quantitative Structure-Activity Relationships. 1991 10(4) 306-332. 

Approximately 7% of all live-born humans bear birth defects. This value may be as high as 10% if children are evaluated to age 10 years to include subtle structural or functional deficits such as minimal brain dysfunction or attention deficit disorders. More than 560 000 lives out of 3 million births per year in the United States are lost through infant death, spontaneous abortion, stillbirths, and miscarriage due presumably to defective fetal development. The relative contributions to human teratogenesis have been estimated as follows known germinal mutations, 20% chromosomal and gene aberrations, 3-5% environmental causes such as radiation, <1% infections, 2% or 3% maternal metabolic imbalance, 1% or 2% drugs and environmental chemicals, 4% or 5% contributions from maternal dietary deficiencies or excesses and... 

Frierson MR, Mielach FA, Kochhar DM. Computer-automated structure evaluation (CASE) of retinoids in teratogenesis bioassays. Fundam Appl Toxicol 1990 14 408-28. 

Teratogenesis—induction of structural or functional development abnormalities by exogenous factors acting during gestation interference with normal embryonic development... 

Nan H (1994) Retinoid teratogenesis toxicokinetics and structure specificity. In Bolt HM, HeUman B, Denker L (eds) Use of mechanistic information in risk assessment (Archives in Toxicology, Supplement 16), Springer-Verlag, Berlin, pp. 118-127. 

Horton, C. and Maden, M. (1995) Endogenous distribution of retinoids during normal development and teratogenesis in the mouse embryo. Dev. Dynam. 202,312-323. Spom, M. B., Dunlop, V. M Newton, D. L., and Henderson, N. R. (1976) Relationships between structure and activity of retinoids. Nature 263,110-113. 

Since the piperidines behave in a specific way and are teratogenic, they also fulfill specific criteria for teratogenesis [23, 24, 38, 70, 85]. The structural characteristics of these piperidines need to be determined and their main differences outlined to be able to find out their mechanism of action, as fetal movement and malpositioning. The birth defects caused by Conium maculatum are the same, and their biological activities occur by a similar mechanism of action [16,52, 65,66,70]. As usual with biological active compounds one use to characterize the toxicity into acute and chronic forms. The peripheral actions of coniine are similar to those of nicotine, but it produces more pronounced paralysis of the central nervous system and of the skeletal muscle nerve [65, 70]. 

Teratogenesis Brain. An examination of development of neurons in the nematode Caenorhabditis elegans, found that the polarity of the synaptic structure is dependent on mi/o-inositol monophasphatase, and enzyme... 

Enslein, K., Lander, T.R. and Strange, J.R. 1983b. Teratogenesis A statistical structure-activity model. J. Teratog. Carcinog. Mutag. 3 289-309... 

Lammer EJ, Armstrong DL (1992) Malformations of hindbrain structures among humans exposed to isotretinoin (13-cw-retinoic acid) during early embryogenesis. In GM Monis-Kay (ed.) Retinoids in normal development and teratogenesis. Oxford University Press, Oxford, 281-295... 

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