Fetus teratogenesis

F. Reproductive toxins Chemicals which affect the reproductive capabilities including chromosomal damage (mutations) and effects on fetuses (teratogenesis) ... 

Reproductive Toxicology (mammalian) The study of the effects of chemicals on the adult reproductive and neuroendocrine systems, the embryo, foetus, neonate and prepubertal mammal. Reproductive Toxins Tire tenn refers to a specific target organ characterization of effect. These are chemicals which affect the reproductive capabilities including chromosomal damage (mutations) and effects on fetuses (teratogenesis). Signs and symptoms include birth defects sterility. Examples are lead and DBCP. 

In addition to direct effects of chemical compounds on the fetus, metabolic disturbances in the mother, such as diabetes or hyperthermia, or deficiencies of calories or specific nutrients such as vitamin A, zinc, and folic acid may lead to teratogenesis. Compounds that inhibit placental functions may also induce malformations, e.g., by inhibiting placental circulation. For example, hydroxyurea disrupts the placental circulation and induces malformations. In addition, it also induces DNA damage. 

Although low risks of teratogenesis, including risk of neural tube defects have been reported for several antiepileptics it should be realized that uncontrolled epilepsy poses far more risks for the fetus. 

Teratogenesis involves interference with the normal development of either the embryo or fetus in utero, giving rise to abnormalities in the neonate. This interference may take many forms, and there is therefore no general mechanism underlying this type of response. Many of the toxic effects described elsewhere in this book may be teratogenic in the appropriate circumstances. 

Teratogenesis is the specific interference with the development of the embryo or fetus. 

Retinoids increase cellular mitotic activity, DNA and RNA synthesis, and protein synthesis. The primary toxicity of concern is female-mediated teratogenesis. Isotretinoin alters cell differentiation and placement in developing fetuses that are exposed to it in the first... 

Dencker L, Danielsson BR. 1987. Transfer of drugs to the embryo and fetus after placentation. In Nau H, Scott WJ Jr, eds. Pharmacokinetics in Teratogenesis. Vol. I. Interspecies Comparison and Matemal/Embryonic-Fetal Drug Transfer, 55-69. 

Teratogens are chemical species that canse birth defects. These usually arise from damage to embryonic or fetal cells. However, mntations in germ cells (egg or sperm cells) may canse birth defects, snch as Down s syndrome. The biochemical mechanisms of teratogenesis are varied. These include enzyme inhibition by xenobiotics deprivation of the fetus of essential substrates, such as vitamins interference with energy supply or alteration of the permeability of the placental membrane. 

The AHR is not merely important in mediating TCDD-initiated teratogenesis, but necessary. Studies using Ahr mice unequivocally demonstrate this requirement for the AHR. For example, fetuses from Ahr dams exposed to a high dose of TCDD, display minimal incidences of cleft palate and hydrtMiephrosis when compared to fetuses (Lin et al. 2001 Mimuraet al. 1997 Peters et al. 1999). 

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