Pulmonary lesions produced by nephrotoxic anti-placenta serum.
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The distribution of zinc between the mother and the fetoplacental unit, and its placental transfer, were studied using stable and isotopic zinc in unanaesthetized pregnant guinea pigs and an in situ perfusion preparation. The concentration of stable zinc in fetal plasma and skeletal muscle was higher than that in the maternal tissues: 2.0 compared with 1.4 micrograms/ml and 84 with 49 ng/mg dry weight, respectively. The placenta and maternal and fetal liver had similar zinc concentrations: 90, 75 and 88 ng/mg dry weight, respectively. The ability of the placenta to concentrate 65Zn, measured 1 h after a single intravenous injection into the unanaesthetized mother, was comparable with that of the maternal liver. Maternal-fetal mass transfer of zinc was directly related to maternal plasma zinc concentrations from 0.7 to 24.1 micrograms/ml (b = 2 ng X min-1 X g-1 X microgram-1, r = 0.92). At physiological plasma levels, the calculated transfer would supply the fetus with 0.12 mg zinc/day, similar to the accretion rate over the last trimester. Placental transfer of zinc was not influenced by the concentration of zinc in the placental perfusate. Extraction of zinc from the perfusate was also slow, and partly by absorption. Maternofetal transfer of zinc was directly related to both uterine and umbilical blood flows. The high concentration of zinc in the syncytium, relative to both maternal and fetal plasma levels, suggests active uptake at the maternal surface, combined with a slow release into the fetus, down a concentration gradient.
An attempt has been made to show that the increase in enzyme activities in sera of pregnant women found with glucose-6-phosphate and adenosine 5'-monophosphate as substrates (described as glucose-6-phosphatase and 5'-nucleotidase) was due to the increase in alkaline phosphatase. The three enzyme activities has pH optima and heat stability characteristics of alkaline phosphatase. The response to the action of inhibitors and activators was typical for alkaline phosphatase. There was an identical increase in all three enzyme activities during pregnancy. As a control similar investigations were made with liver and placental tissue extracts.
Four African-American girls aged 14 months to 93 months developed breast or pubic hair 2 to 24 months after starting the use of estrogen or placenta-containing hair products. Discontinuing the use of the hair products resulted in regression of the breast or pubic hair. Serum gonadotropins and estradiol levels were variable. No other cause for early sexual development was noted in these girls.
Placenta expresses various lipase activities. However, a detailed characterization of the involved genes and proteins is lacking. In this study, we compared the expression of endothelial lipase (EL) and LPL in human term placenta. When placental protein extracts were separated by heparin-Sepharose affinity chromatography, the EL protein eluted as a single peak without detectable phospholipid or triglyceride (TG) lipase activity. The major portion of LPL protein eluted slightly after EL. This peak also had no lipase activity and most likely contained monomeric LPL. Fractions eluting at a higher NaCl concentration contained small amounts of LPL protein (most likely dimeric LPL) and had substantial TG lipase activity. In situ hybridization studies showed EL mRNA expression in syncytiotrophoblasts and endothelial cells and LPL mRNA in syncytiotrophoblasts. In contrast, immunohistochemistry showed EL and LPL protein associated with both cell types. In mouse placentas, lack of LPL expression resulted in increased EL mRNA expression. These results suggest that the cellular expression of EL and LPL in human placenta is different. Nevertheless, the two lipases might have overlapping functions in the mouse placenta. Our data also suggest that the major portions of both proteins are stored in an inactive form in human term placenta.
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The effect of human placenta hydrolysate (Laennec) on residual liver regeneration after about 70% partial hepatectomy (PH) in normal and CCl4-induced cirrhosis rats was examined. Both intravenous or subcutaneous injections of Laennec increased the regeneration rate of the residual liver after PH in normal rats. Intravenous injection of Laennec inhibited the decrease of liver total protein, and it decreased the level of serum transaminase (GOT, GPT). The regeneration rate of the residual liver after PH in CCl4-induced cirrhosis (CCl4-PH) rats increased by intravenous or subcutaneous injection of Laennec. Laennec also inhibited the increase of serum GOT caused by CCl4-PH. In the pathological examination of the regenerating liver, intravenous injection of Laennec minimized the pathological changes caused by PH or CCl4-PH such as vacuolation and necrosis in the hepatocytes. The enhancement of cytoplasma regeneration in hepatocytes was noticed by intravenous injection of Laennec, but that by subcutaneous Laennec was slight. Intravenous injection of Laennec also minimized the lipid deposition in liver caused by CCl4-PH. Laennec had no effect on the pseudolobule formation caused by CCl4. Thus, the effect of intravenous injection of Laennec on the liver regeneration in PH rats was much more potent than that by the subcutaneous injection.
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We have investigated the effect of a therapeutic agent for liver disease, Laennec, on the GOT leakage from freshly isolated and primary cultured rat hepatocytes which were treated with CCl4. By treatment with Laennec together with CCl4, the GOT leakage from isolated hepatocytes increased and that from cultured hepatocytes decreased, compared to those incubated only with CCl4. The results suggest that it is better to use primary cultured hepatocytes than to use freshly isolated hepatocytes to evaluate therapeutic agents for liver disease.
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