Placental

ANTIBIOTICS - BETA-LACTAMS - PENICILLINS AND OTHERS] (Vol 3) Placental GH [109675-94-7]... 

Placental lactogens Plagioclase Planchette counting Planck s constant Planck s law Plane tree Planiblock Planography Plantago ovata Plantains... 

When a mminant is bom, it consumes colostmm within a few hours. Colostmm contains antibodies from the mother s milk that serve to immunize the neonate against disease (37). These antibodies can be absorbed by the neonate only within the first few days of its life there is no placental transfer of antibiotics in mminants (37). 

Chorionic Somatomammotropin. Three genes encode human chorionic somatomammotropin [11085-36-2] (hCS). These are located within a cluster of genes on human chromosome 17 which code for pituitary growth hormone [12629-01 -5] (GH-N), placental GH [109675-94-7J (GH-V), and three hCS molecules, ie, hCS-A, hCS-B, and hCS-V (1 3), also referred to as human placental lactogens. All of these molecules ate closely related to GH in stmcture (Fig. 1). Placental lactogens also exist in rodents and mminants however, these hormones are more closely related to prolactin than GH. 

Fig. 1. Primary stmcmre of the human growth hormone family of proteins. GH-N = pituitary GH GH-V = placental GH variant ...

Specific barriers may serve to limit dmg distribution. The placental barrier is of obvious importance to dmg action in the fetus. Dmg transfers across the placenta primarily by Hpid solubiHty. Hence, this barrier is not particularly restrictive. Similarly, the Hpid solubiHty of a dmg is a primary deterrninant in access to the brain and cerebrospinal fluid. Generally, hydrophilic or charged dmgs can also penetrate to these latter areas, but the result is slow and incomplete. The blood brain barrier is composed of cells having tight junctions which are much less permeable to solutes than are the endotheHal cells of other tissues. 

Myxedema and goiter are the main conditions for which thyroid preparations are indicated. The treatment of cretinism is difficult because it is recognized only at or after birth. Even if this disease could be diagnosed m utero, thyroid hormones do not readily cross the placental barrier. In addition, the fetus, as does a premature infant, rapidly deactivates the thyroid hormones. The halogen-free analogue DlMlT [26384-44-7] (3), which is resistant to fetal deiodinases, may prove useful for fetal hypothyroidism (cretinism). 

Puromycin. Puromycin (19), elaborated by S. alboniger (1—4), inhibits protein synthesis by replacing aminoacyl-tRNA at the A-site of peptidyltransferase (48,49). Photosensitive analogues of (19) have been used to label the A-site proteins of peptidyltransferase and tRNA (30). Compound (19), and its carbocycHc analogue have been used to study the accumulation of glycoprotein-derived free sialooligosaccharides, accumulation of mRNA, methylase activity, enzyme transport, rat embryo development, the acceptor site of human placental 80S ribosomes, and gene expression in mammalian cells (51—60). 

Human exposure to environmental contaminants has been investigated through the analysis of adipose tissue, breast milk, blood and the monitoring of faecal and urinary excretion levels. However, while levels of persistent contaminants in human milk, for example, are extensively monitored, very little is known about foetal exposure to xenobiotics because the concentrations of persistent compounds in blood and trans-placental transmission are less well studied. Also, more information is needed in general about the behaviour of endocrine disruptive compounds (and their metabolites) in vivo, for example the way they bind to blood plasma proteins. 

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. 

Animal nutritionists have developed formulas to guide them in recommending the amount of food to feed animals in captive situations such as in zoos. First, the number of calorics needed to maintain the animal while at rest is determined—this is called the basal metabolic rate (BMR). In general, a reptile s BMR is only 15 percent that of a placental mammal, while a bird s is quite a bit higher than both a reptile s and a mammal s. For all animals, the number of calories they should receive on a maintenance diet is twice that used at the basal metabolic rate. A growing animal should receive three times the number of calories at the BMR, while an animal in the reproductive phase should receive four to six times the BMR. 

Cadherins are a superfamily of Ca2+-sensitive cell-cell adhesion molecules, which cause homophilic cell interactions. Cadherins can be divided into different subfamilies, namely, classical cadherins, desmosomal cadherins, protocadherins, and nonconventional cadherins (7TM cadherins, T-cadherin, FAT). Classical cadherins are often denoted by a prefix reflecting their principal expression domains e.g., E is epithelial, N is neuronal, and P is placental. However, this classification is not stringent, as for instance E-cadherin can also be found in certain neuronal tissues, and N-cadherin is also found in epithelial cells. Among the desmosomal cadherins, two subfamilies can be distinguished the desmocollins 1-3 and the desmogleins 1-4. 

After administration of a single oral dose of dibutyltin diacetate of 22 mg/kg body weight to pregnant rats on day 8 of gestation, both dibutyltin and monobutyltin were detected in the embryos, indicating placental transfer (Noda et al., 1994). Nakamura et al. (1993) also detected dibutyltin in embryos after dosing the mother orally on days 7-17 of gestation. 

In recent in vitro studies, an aromatase inhibiting effect on human placental microsomal extracts has been demonstrated with both tributyltin chloride and dibutyltin dichloride (Heidrich et al, 2001 Cooke,... 

Placental transfer of methyl parathion was demonstrated following oral administration to pregnant rats 1-3 days before parturition (Ackermann and Engst 1970). 

Data from a single study in dogs suggest that hepatic first-pass metabolism may limit systemic availability of the parent compound following oral exposure (Braeckman et al. 1983). Placental transfer of methyl parathion was demonstrated in pregnant rats 1-3 days before parturition. Thirty minutes after administration, both methyl parathion and methyl paraoxon were found in fetal brain, liver, and muscle methyl parathion, but not methyl paraoxon, was detected in placenta and maternal liver (Ackermann and Engst 1970). Methyl parathion binds reversibly to serum albumin, but is readily distributed to the tissues (Braeckman et al. 1980, 1983). 

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