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PubMed · 2937020

Paternal contributions to birth defects.

Abstract

The question of the extent of paternal contributions to birth defects and adverse reproductive outcomes gained new urgency with the concerns of Vietnam veterans exposed to Agent Orange. There is well-established evidence for the occurrence of certain autosomal dominant sporadic mutations in the offspring of older fathers. Paternal nondisjunction at meiosis or mitosis accounts for a significant proportion of chromosomal errors such as trisomy 21. Certain chromosomal abnormalities in males also contribute to adverse reproductive outcomes in relation to repetitive spontaneous abortion and infertility. The question of whether or not teratogens can act through the male is complex. While certain suggestive evidence is reviewed here, conclusive data are yet to be found. Yet, we must remember that it was not long ago that the placenta was assumed to be an impenetrable barrier between mother and fetus. This field is ripe for further well-designed and careful investigation.

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BibTeXRIS

F L Cohen. 1986. Paternal contributions to birth defects.. https://pubmed.ncbi.nlm.nih.gov/2937020/

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2,4,5-Trichlorophenoxyacetic acid promotes somatic embryogenesis in the rose cultivar "Livin' Easy" (Rosa sp.).

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2,4,5-Trichlorophenoxyacetic Acid↗