Study of developmental abnormalities and deaths after human zygote exposure

Csaba Siffel, Andrew E. Czeizel

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Experimental studies indicated that the mouse zygote is susceptibel to experimental induction of developmental anomalies including defects (mainly hydrops), growth retardation and mid- and late-gestational death with certain mutagenic agents. The material of the Hungarian Optimal Family Planning Program is appropriate to check this finding in a human material because participants were asked to visit the coworkers of the Program immediately after the first missed menstrual period and data concerning potentially hazardous environmental factors were obtained. At that time participants were immediately after the pre-and implantation period and they had no knowledge about their pregnancy outcomes. In 1994 the data of their pregnancy outcomes are available. Of 5453 evaluated pregnancies, 1167 were selected for this study because they visited the coworkers of the Program within 28 days post conception. Of 1167 pregnancies, 316 (27%) were exposed to some environmental factors, mainly drugs. A mild intrauterine growth retardation was found in the exposed group. The rate of congenital abnormalities and infant death did not differ between the exposed and unexposed groups. The detailed analysis of different congenital abnormality groups also did not show any significant difference between the exposed and unexposed groups. These negative results are explained by the fact that the observed environmental factors are not mutagenic, at least not in the dosage which was used, or the human zygote is not sensitive to mutagenic agents in the post-conceptional days.

Original languageEnglish
Pages (from-to)293-300
Number of pages8
JournalMutation Research/Environmental Mutagenesis and Related Subjects
Volume334
Issue number3
DOIs
Publication statusPublished - Jun 1995

Keywords

  • Developmental abnormality
  • Human zygote

ASJC Scopus subject areas

  • Toxicology
  • Genetics

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