Specific and Non-Specific Developmental Effects

  • Ludwig Machemer
  • Ulrich Schmidt
  • Beate Holzum

Abstract

Embryo damage can arise in a number of different ways. Essentially two possibilities exist:
  1. A.

    Noxae exert specifically developmental toxicity. In such cases the embryo often demonstrates greater sensitivity than the maternal organism, and embryotoxic effects show no correlation with maternal toxicity. The effects are often described as specific or primary embryotoxicity.

     
  2. B.

    Embryo damage results from maternal damage, and a relationship between a female response and the offspring can be demonstrated. These effects are often described as non-specific, or secondary. However, the mechanism is not usually known, so that in principle a direct or specific damage to the embryo cannot be ruled out. All that can be stated in the majority of cases is that maternal and developmental toxicity are correlated, i.e., there is a correspondence between the sensitivity of the mother and that of the embryo.

     

Keywords

Fetal Weight Developmental Toxicity Maternal Toxicity Embryotoxic Effect Rare Malformation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. DFG Deutsche Forschungsgemeinschaft (1990) Kriterien zur Beurteilung von Studien zur Reproduktionstoxizität mit Pflanzenschutzmitteln. Mitteilung XVIII der Kommission für Pflanzenschutz-, Pflanzenbehandlungs-und Vorratsschutzmittel, VCH Verlagsgesellschaft mbH, Weinheim.Google Scholar
  2. Frankos VH (1985) FDA Perspectives on the use of teratology data for human risk assessment. Fund Appl Toxicol 5: 615–625.CrossRefGoogle Scholar
  3. Fraser FC (1963) Experimental teratogenesis in relation to congenital malformations in man. In: Congenital Malformations. Papers and Discussions presented at the Second International Conference New York, July 14–19, The International Medical Congress Ltd, pp 277-287Google Scholar
  4. Hart WL, Reynolds RC, Krasavage WJ, Ely ThS, Bell HR, Raleigh RL (1988) Evaluation of developmental toxicity data: A discussion of some pertinent factors and a proposal. Risk Analysis 8/1: 59–69.CrossRefGoogle Scholar
  5. Jusko WJ (1972) Pharmacodynamic principles in chemical teratology: dose-effect relationships. J Pharmacol Exp Ther 183: 469–480.PubMedGoogle Scholar
  6. Jusko WJ (1973) Pharmacokinetic principles in chemical teratology. Proc Study of Drug Toxicity XIV: 9–19.Google Scholar
  7. Karaofsky DA (1965) Mechanism of action of growth-inhibiting drugs. In: Wilson JG, Warkany J (eds) Teratology: Principles and Techniques, Univ. of Chicago Press, Chicago.Google Scholar
  8. Matringe M, Camadro J-M, Labbe P, Scalla R (1989) Protoporphyrinogen oxidase inhibition by three peroxidizing herbicides: Oxadiazon, LS 82-556 and M&B 39279. FEBS Lett 245: 35–38.PubMedCrossRefGoogle Scholar
  9. Neubert D, Chahoud I, Platzek T, Meister R (1987) Principles and problems in assessing prenatal toxicity. Arch Toxicol 60: 238–245.PubMedCrossRefGoogle Scholar
  10. Schwetz BA, Tyl RW (1987) Consensus Workshop on the Evaluation of Maternal and Developmental Toxicity, Work Group III Report: Low dose extrapolation and other considerations for risk assessment — models and applications. Teratogen Carcinogen Mutagen 7: 321–327.CrossRefGoogle Scholar
  11. Setzer RW, Rogers JM (1991) Assessing developmental hazard: The reliability of the A/D ratio. Teratology 44: 653–665.PubMedCrossRefGoogle Scholar
  12. Wang GM, Schwetz BA (1987) An evaluation system for ranking chemicals with teratogenic potential. Teratogen Carcinogen Mutagen 7: 133–139.CrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1992

Authors and Affiliations

  • Ludwig Machemer
  • Ulrich Schmidt
  • Beate Holzum

There are no affiliations available

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