Placenta copper

Diamine Oxidases. Diamine oxidases are enzymes that also oxidize amines to aldehydes. The preferred substates are aliphatic diamines in which the chain length is four (putrescine) or five (cadaverine) carbon atoms. Diamines with carbon chains longer than nine will not serve as substrates but can be oxidized by monoamine oxidases. Secondary and tertiary amines are not metabolized. Diamine oxidases are typically soluble pyridoxal phosphate-containing proteins that also contain copper. They have been found in a number of tissues, including liver, intestine, kidney, and placenta. 

Tabacova, S., Baird, D.D., Balabaeva, I., Lolova, D., Petrove, I. (1994). Placental arsenic and cadmium in relation to lipid peroxides and glutathione levels in maternal-infant pairs from a copper smelter area. Placenta 15 873-81. 

Copper and Certdoplasmin in the Newborn and in Children. Tissue copper concentrations at birth are relatively high, particularly in the liver. However, concentration of copper in serum is lower at birth than at any other time. It is particularly high in the mother, approximately five times as much as that of the newborn (118). It is believed that the difference between the mother and the baby is attributable to the diminished capacity of the newborn to synthesize ceruloplasmin (16). Since unbound copper can pass the placental barrier, its concentration is the same on both sides of the placenta, but this is not the case with the protein-bound copper ceruloplasmin, which constitutes the majority of copper in serum. 

Metallothionein in the gastrointestinal mucosa plays a role in the gastrointestinal transport of cadmium. Its presence in cells of the placenta impairs the transport of cadmium from maternal to fetal blood and across blood-brain barriers, but only when the concentration of cadmium is low. Newborns are virtually cadmium free, whereas zinc and copper are readily supplied to the fetus. Rapid renal concentration occurs mainly during the early years of life. 

Poria placenta (particularly tolerant to copper and zinc compounds). 

The rat ceruloplasmin cDNA clone described above was further used to identify extrahepatic sites of ceruloplasmin gene expression in the rat. Although the liver was originally postulated to be the sole tissue source of ceruloplasmin (189), the above study resulted in the detection of ceruloplasmin mRNA in the choroid plexus, yolk sac, placenta and testis of the rat. Since these tissues are situated at the interface between adjacent extracellular compartments, it has been suggested that ceruloplasmin may be involved in maintaining copper homeostasis in these compartments (189). 

Goyer and Cherian (1992) measured cadmium, zinc and copper, and metallothionein content of human placentas from 55 uncomplicated, full-term deliveries. The mothers ages ranged from 22 to 39 years, mean 29 years. All were current nonsmokers, but 16 (30%) acknowledged smoking in the past. None were on medication apart from iron and vitamin supplements. For 43 it was the first delivery, for 9 the second, for 1 the third, and for 2 the fourth. Samples of maternal and fetal blood were not obtained. Metals were measured by atomic absorption spectrophotometry and metallothionein by a silver saturation method (Scheuhammer and Cherian 1986). The results are shown in Table 1. Zinc levels of placentas were almost the same as those in the Kuhnert et al. (1988) study, but copper levels were considerably lower. No other comparable measurements of metallothionein were found in the literature. There is a strongly positive correlation between... 

Table 1. Cadmium (Cd), zinc (Zn), copper (Cu), and metallothionein (Mt) content of 55 human placentas. (From Goyer et al. 1992)...

III. Interactions in Placenta Between Cadmium, Zinc and Copper, and Metallothionein... 

Experimental studies have shown that cadmium can induce metallothionein synthesis in the placenta, particularly in trophoblasts. Metallothionein in the placenta binds the essential trace metals, zinc and copper. The mechanism whereby essential metals are preferentially transported to the fetus and cadmium retained is not known. Experimental studies have shown that exposure of pregnant animals to high levels of cadmium early in pregnancy is teratogenic. Human studies suggest maternal cadmium exposure may reduce fetal birth weight and that this may be an indirect effect of zinc deprivation that occurs with cadmium exposure. 

Mahaffey KR, Goyer R, Haseman JK (1973) Dose-response to lead ingestion in rats fed low dietary calcium. J Lab Clin Med 82 92-100 Manci EA, Blackburn WR (1987) Regional variations in the levels of zinc, iron, copper, and calcium in the term human placenta. Placenta 8 497-502 Markovac J, Goldstein GW (1988) Lead activates protein kinase C in immature rat brain microvessels. Toxicol Appl Pharmacol 96 14-23 McMichael AJ, Vimpani GV, Robertson EF, Baghurst PA, Clark PD (1986) The Port Pirie study maternal blood lead and pregnancy outcome. J Epidemiol Community Health 40 18-25... 

Mobile phase M, = toluene-chloroform (50 1) A/j = benzene-methyl isopropylketone (50 1) Mi = methanol-water-acetic acid (50 30 4). Conditions Ascending technique, run 15 cm. layer thickness 0.25 mm, activation at 120°C for 30 min. Detection (a) metal dithizonates were self detected, (b) 5% aqueous copper sulfate solution for metal diethyidithiocarbamates and (c) 0.25% PAN [l-(2-pyridylazo)-2-naphthol solution) in methanol followed by exposure to ammonia vapors for metal ions. Remarks (1) Best separations on RP-18 with My (2) The extracts of complexes of metals originating from biological samples require careful protection from environmental contamination and (3) The developed TLC method was applied for analysing human placentas collected from patients of the obstetrics Clinic in Tychi (Poland) for Pb. Cd, Zn, Cu, Ni, Mn. and Co content. 

If the placenta is affected by the mutant gene, heterozygous carrier females will have to be identified and therapy begun to ensure adequate transport of copper to the developing fetus. 

The copper concentrations of the kidneys, spleen, pancreas, and placenta of the diseased fetus were significantly higher than those from controls. Therefore, the gene mutation that occurs in the steely-hair syndrome may affect the copper transport system of organs other than the intestine. 

The highly homologous Wilson disease P-type ATPase (ATP7b) and the Menkes s P-type ATPase (ATP7a) differ only in their tissue expression and both function to move copper from one intracellular compartment to another. The ATP7a is predominantly located in the placenta, blood-brain barrier, and gastrointestinal tract and hence any mutation in the Menkes s P-type ATPase results in a copper deficiency in the fetus, brain, and tissues. In contrast, the Wilson s disease P-type ATPase is expressed in the liver and mutations in this culminate in profound copper overload of the liver because of the inability to shuttle copper into the trans golgi network for incorporation into ceruloplasmin. The excess copper is stored in the liver and eventually leaks out in the serum where it is deposited within sensitive tissues the eye and brain. The psychiatric... 

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