Fetus and

Nakamura T, Noda T, Saitoh M, Morita S (1993) Determination of di- and mono-n-butyltin compounds in fetuses and some organs from pregnant rats treated Mth di-rt-butyltin diacetate. EiseiKagaku, 39(3) 219-225. 

Comar, C.L., Whitney, I.B. and Lengemann, F.W. 1955 Comparative utilization of dietary Sr and calcium hy the developing rat fetus and growing rat. Proceedings of the Society for Experimental Biology 88 232-236. 

Following single dermal applications of 10 mg/kg of radiolabeled methyl parathion to pregnant rats, methyl parathion was found to be widely distributed to all major tissues and organs. Concentrations were highest in plasma and kidney, maximum levels measured 2 hours postapplication. Peak levels in liver, brain, fetus, and placenta, were measured 2 to 10 hours later, at which times the highest concentration of methyl parathion was in the fetus (Abu-Quare et al. 2000). 

Oral treatment of pregnant dams with 0.25 /xg (or more) /kg/day of 2,3,7,8-tetrachlorodibenzo-p-dioxin for 10 days during gestation resulted in adverse effects on rat development. No adverse effects were seen at the 0.125 ju,g/kg/day. When C-2,3,7,8-tetrachlorodibenzo-p-dioxin (2.99 fjLc/mg) was given at 2 /xg/kg/day there was activity, primarily in liver and to a lesser extent, in fat and brain. When a single oral dose of 200 /Ag/kg was administered on gestation days 16, 17, or 18 and was followed 6 hours later with tissue sampling, the label was also observed in the fetus and placenta. Placenta had approximately twice as much label as the fetus. 

The high demand for glucose by the fetus and fot synthesis of lactose in lactation can lead to ketosis. This may be seen as mild ketosis with hypoglycemia in women, but in lactating cattle and in ewes cattying twins thete may be vety pronounced ketosis and profound hypoglycemia. 

The POMC protein is processed differendy in the anterior lobe than in the intermediate lobe. The intermediate lobe of the pituitary is mdimentary in adult humans, but it is active in human fetuses and in pregnant women during late gestation and is also active in many animal species. Processing of the POMC protein in the peripheral tissues (gut, placenta, male reproductive tract) resem-... 

Fetal hemoglobin Is the major hemoglobin of the red cells of the fetus and the newborn. It has the characteristic property of being resistant to denaturatlon by alkali Hb-F Is composed of two a-chalns (the same as In Hbs A and A2) and two... 

In the U.S., the central nervous system syndrome is usually more common among children, and the gastrointestinal syndrome is more prevalent in adults. Exposure to lead is also linked to decreased fertility in men. Lead is a probable human carcinogen, based on sufficient animal evidence. Populations at increased risk of toxicity from exposure to lead include developing fetuses and young children, individuals with decreased kidney function, and children with sickle-cell anemia. 

This section discusses potential health effects from exposures during the period from conception to maturity at 18 years of age in humans, when all biological systems will have fully developed. Potential effects on offspring resulting from exposures of parental germ cells are considered, as well as any indirect effects on the fetus and neonate due to maternal exposure during gestation and lactation. Relevant animal and in vitro models are also discussed. 

Finally, most of the imprinted genes known to date are expressed and imprinted in the placenta. Other imprinted genes are exclusively imprinted in the placenta but not in the fetus, and these may have a role specifically in placental growth or development (Engemann et al 2000). 

With disruption of this barrier, molecules such as albumin freely enter the brain and ions and water follow. Because the brain lacks a well-developed lymphatic system, clearance of plasma constituents is slow, edema occurs, and intracranial pressure rises. At lower levels of exposure, subtle dysfunction of the blood-brain barrier may contribute to neurobehavioral deficits in children (Bressler and Goldstein 1991 Goldstein 1993). The particular vulnerability of the fetus and infant to the neurotoxicity of lead may be due in part to immaturity of the blood-brain barrier and to the lack of the high-affinity leadbinding protein in astroglia, which is discussed later in this section. Results of measurements of transendothelial electrical resistance across the blood-brain barrier from mice of various ages showed that lead potentiates cytokines-induced increase in ion permeability of the blood-brain barrier (Dyatlov et al. 

Further research on the relationship between paternal lead exposure and fetal/infant development should be conducted. Additional information on relationships between nutritional deficits and vulnerability of the fetus and child to lead would be valuable. 

NeedlemanHL. 1987a. Low-level lead exposure in the fetus and young child. Neurotoxicology 8 389-393. 

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