Teratogen and physiological effects on organogenesis

A human teratogen is an agent that alters the growth or structure of the developing embryo or fetus, thereby causing birth defects. The first human teratogen identified in 1941 by an ophthalmologist, Norman Gregg, was maternal rubella infection in pregnancy, which produced a triad of defects (cataracts, heart malformations, and deafness) in the infants (Gregg, 1991).  

Teratogens are environmental agents such as drugs, viruses, lack of nutrients, and physical or chemical elements that upon contact with embryo/fetus can cause congenital anomalies, generating permanent functional or morphological changes in the new-born (Shepard, 1982).

Several factors that determine the teratogenicity of an exposure have been set forth. These include, but are not limited to, the following: Abnormal development produced by a teratogenic exposure is manifested as death, malformation(s), growth retardation, or a functional disorder. These include neurologic impairments, such as mental retardation, and long-term effects on cognition and behaviour that may appear later in childhood.

A second principle of teratology states that susceptibility to teratogenesis varies with the developmental stage at the time of exposure, and a third claims that manifestations of abnormal development depend on dose and duration of a teratogenic exposure. These indicate that not all exposures deemed as teratogenic are actually teratogenic all the time; the timing and dose of a particular exposure during pregnancy often determine the kind and extent of its teratogenic potential. For example, administration of many established major teratogenic drugs, such as isotretinoin, valproic acid, warfarin, or high-dose methotrexate, in specific gestational windows in the first trimester is associated