Organogenesis during

Ema M, Kurosaka R, Amano H, Ogawa Y (1996) Comparative developmental toxicity of di-, tri- and tetrabutyltin compounds after administration during late organogenesis in rats. Journal of Applied Toxicology, 16(1) 71-76. 

EI Dupont deNemours Co. 1973. Maternal toxicity, embryotoxicity and teratogenic potential of neoprene accelerators applied to skin of rats during organogenesis. OTS0556789. Sect 8D. 

The critical time for organogenesis is during the first eight weeks of pregnancy thus, the risk for birth defects is highest during the first trimester. 

Exposure to the fetus in the first 2 weeks after conception may have an all or nothing effect (i.e., could destroy the embryo or have no ill effect). Exposure during the period of organogenesis (18 to 60 days postconception) may result in structural anomalies (e.g., methotrexate, cyclophosphamide, diethylstilbestrol, lithium, retinoids, thalidomide, certain antiepileptic drugs, and coumarin derivative). 

Globally, those experiments with knockout mice suggest that the implication of more than one member of the nuclear receptor family may have prominent effects in organogenesis, even if their expression is for a brief period during embryonic life. The mice with double or triple knock-outs, lacking two or three receptors, will surely contribute to finally clarifying the roles of each hormone and each receptor. 

Treatment of rats with cypermethrin up to 8 mg/kg/day produced no malformations [140]. Maternally toxic dose level of bifenthrin did not produce adverse effects on embryonic development in rats [141], A rabbit teratology study with 30 or 90 mg/kg/day tetramethrin during fetal organogenesis demonstrated no adverse effects on skeletal or external development [137]. 

Ellington, S. (1980). In vivo and in vitro studies on the effects of maternal fasting during embryonic organogenesis in the rat. J. Reprod. Fertil. 60 383-388. 

Short RD, Minor JL, Ferguson B, et al. 1976. The developmental toxicity of ethylene dibromide inhaled by rats and mice during organogenesis. US Environmental Protection Agency. Washington, D.C. US Environmental Protection Agency. EPA-560/6-76-018 NTIS no. PB-256659, 11. 

Yang HY, Lee QP, Rettie AE, Juchau MR. 1994. Functional cytochrome P4503A isoforms in human embryonic tissues expression during organogenesis. Mol Pharmacol 46 ... 

Segment 11 teratogenicity study. This concentrates on the most sensitive part of gestation, from the time of implantation imtil major organogenesis is complete. This is the period during which a test substance is most likely to cause malformation of the embryo. Exposure of the mother to the test substance is usually confined to this period. Conventionally, the study is conducted in rats and rabbits. Rabbits are intolerant to antibiotics and the mouse is an acceptable alternative in most cases. 

Exposure of rats to DEHA during organogenesis caused an increased frequency of variations and retardations in the fetuses at doses below the maternally toxic range." ... 

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