Transfer and accumulation of cadmium, and the level of metallothionein in perfused human placentae

Boadi, William Y.; Yannai, S.; Urbach, Jacob; Brandes, Joseph M.; Summer, K

doi:10.1007/bf01968966

Cited by 49 publications

(19 citation statements)

References 24 publications

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“…Metallothionein levels in the placenta ob served in our study are in agreement with the few reports in the literature on a reduced number of human samples [24,25], This low-molecular-weight cystein-rich protein is thought to play a role in cellular zinc homeo stasis and to provide protection from toxic heavy metals such as cadmium [35], Its func tion in the placenta has yet to be elucidated but it may serve as a temporary zinc reservoir helping to regulate the zinc flow to the fetus while restricting toxic metal transfer [25,36], In our study, placental metallothionein levels did not relate to placental zinc or to any matemal/cord zinc-related component. There fore, in healthy pregnant women, the possible regulatory role of placental metallothionein in maternal-fetal transfer of zinc is unclear.…”

Section: Effect O F Maternal Serum Zinc Levelssupporting

confidence: 80%

Maternal, Placental and Cord Zinc Components in Healthy Women with Different Levels of Serum Zinc

Zapata

Melo

Donangelo³

1997

Neonatology

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Serum zinc is known to decrease during pregnancy, but the range of individual values at the end of normal gestation may be considerably large, with uncertain physiological significance in terms of maternal zinc status and maternal-fetal transfer of zinc. In this study we compared several maternal and cord blood indices of zinc status, placental zinc, placental metallothionein and the relationship between maternal, cord and placental components, in 40 healthy pregnant women at delivery with different levels of serum zinc. Subjects were divided into three groups according to serum zinc using as cutoff points the lower and upper quartile values [LZn, < 7.6 µmol/l (n = 10); MZn, 7.6–10.7 µmol/l (n = 20), and HZn, > 10.7 µmol/l (n = 10)]. Habitual zinc intakes were similar in all groups (average 11.5 mg/day). Considering all women, maternal serum and erythrocyte zinc correlated significantly (r = 0.40; p = 0.021). Maternal erythrocyte zinc was higher (p < 0.01) in HZn compared to the other groups. Maternal and cord values of serum zinc correlated significantly (r = 0.43; p = 0.006). Cord serum zinc values were very similar in LZn and MZn but were higher (p < 0.01) in HZn. Cord erythrocyte zinc levels were similar in all groups and about 20–25% of the maternal values. Cord erythrocyte metallothionein levels were also similar in all groups and similar to maternal values. Comparing the percentage distribution of zinc in maternal and cord serum fractions, major differences were observed in HZn, with zinc in albumin fraction being 70% in cord compared to 56% in maternal serum. There was a higher (p < 0.01) percentage of zinc bound to α₂-macroglobulin fraction in maternal serum of HZn compared to maternal serum of the other groups. Maternal and cord zinc in the albumin fractions correlated significantly (r = 0.48; p = 0.002) particularly in HZn (r = 0.71; p < 0.021). Placental zinc correlated negatively (r = ––0.34; p = 0.035) with zinc in the maternal α₂-macroglobulin fraction, but did not relate to placental metallothionein, which had similar levels in all groups (average 0.28 nmol/g wet tissue). Placental zinc levels were lower (p < 0.01) in HZn. Our results indicate that high levels of maternal serum zinc in healthy women at delivery may be related to maternal tissue zinc redistribution that could favor diffusional components of maternal-fetal transfer of zinc.

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Section: Effect O F Maternal Serum Zinc Levelssupporting

confidence: 80%

Maternal, Placental and Cord Zinc Components in Healthy Women with Different Levels of Serum Zinc

Zapata

Melo

Donangelo³

1997

Neonatology

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“…Six hours after Cd treatment, ultrastructural changes in the placenta included the following: cytoplasmic edema, enlargement of mitochondria and their fragmentation and loss (Levin et al 1981;di Sant'Agnese et al 1983). We have also observed similar changes in mitochondria and other placental organelles, as well as changes in metallothionein level following perfusion of term placental cotyledon with Cd (Boadi et al 1991 ). Thus, Cd appears to induce placental injury and to alter placental function in the rodent and human.…”

Section: Introductionsupporting

confidence: 64%

“…It is therefore conceivable that the effect on hCG secretion was produced by the tissue-bound portion of the metal, that could not be removed by the extensive washing. Evidence for placental tissue accumulation of Cd was reported previously in studies with perfused placenta at term (Boadi et al 1991).…”

Section: Discussionmentioning

confidence: 71%

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Secretion of human chorionic gonadotropin in superfused young placental tissue exposed to cadmium

et al. 1992

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The effect of various concentrations of cadmium (Cd) in levels ranging from 0.75 to 12 micrograms/ml medium, on the secretion of human chorionic gonadotropin (hCG) in first-trimester placental explants, after 6 or 24 h incubation, employing both static and dynamic systems was examined. Later the unbound Cd was washed for 45 min with fresh medium devoid of Cd, followed by superfusion with the latter medium for 75 min, during which time samples were collected for hCG assay. For the superfusion experiments the parameters used for evaluating the hCG secretion pattern were: mean peak amplitude (MPA), pulse frequency (PF) and the area under the hCG secretion curve (AUC). The results indicate that in the dynamic system the hCG secretion increased significantly, and this increase was dose dependent. There was also a dose-related increase in mean total hCG secreted by the explants exposed to Cd. Maximal hCG secretion was observed after 24 h exposure of explants to 6 micrograms of the metal/ml. Both the MPA and AUC parameters showed a statistically significant increase for this dose level. At 12 micrograms/ml, the pulsatile secretion of hCG decreased, the value for the mean hCG secretion being comparable to that observed for 0.75 micrograms/ml. After 6 h incubation, however, there were no significant changes from the control, as judged by all of the above parameters. The levels of hCG secreted by the explants into the media in the static system were not significantly different from their respective controls, for both incubation periods and Cd levels. These results indicate that Cd may affect the normal placental function, as reflected in its hCG secretion pattern.

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“…Such failure of these metals to affect fetal steroidogenesis may be due to the poor transfer into fetuses. For instance, the matured BPB has been reported to interfere with the translocation of Cd into the fetus (Boadi et al, 1991;Ji et al, 2011). It is, therefore, an alternative possibility that the failure of Cd given at GD15 to reduce fetal steroidogenesis is due to the inappropriate choice of dosing time when the BPB is already mature.…”

Section: Resultsmentioning

confidence: 99%

Effect of <i>in utero</i> exposure to endocrine disruptors on fetal steroidogenesis governed by the pituitary-gonad axis: a study in rats using different ways of administration

et al. 2015

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-The effects of endocrine disruptors on testicular steroidogenesis in fetal rats were investigated in a study involving in utero exposure. In the major part of this study, pregnant rats at gestational day (GD)15 were given a single oral administration of the test substance, and then the expression of the following mRNAs in GD20 fetuses was determined: testicular steroidogenic acute-regulatory protein (StAR), a cholesterol transporter mediating the rate-limiting step of steroidogenesis, a ß-subunit of pituitary luteinizing hormone (LH), and a regulator of gonadal steroidogenesis. Among the substances tested, only di(2-ethylhexyl)phthalate (DEHP) reduced the expression of fetal testicular StAR. The others listed below exhibited little effect on fetal StAR: 2,2',4,4'-tetrabromodiphenylether, tributyltin chloride, atrazine, permethrin, cadmium chloride (Cd), lead acetate (Pb) and methylmercury (CH 3 HgOH). None of them, including DEHP, lacked the ability to reduce the expression of pituitary LHß mRNA. The present study also examined the potential of metals as modifiers of fetal steroidogenesis by giving them to pregnant dams in drinking water during GD1 and GD20. Under these conditions, Cd and Pb at a low concentration (0.01 ppm) significantly attenuated the fetal testicular expression of StAR mRNA without a concomitant reduction in LHß. No such effect was detected with CH 3 HgOH even at 1 ppm. These results suggest that: 1) DEHP, Cd and Pb attenuate the fetal production of sex steroids by directly acting on the testis, and 2) chronic treatment during the entire gestational period is more useful than a single administration for determining the hazardous effect of a suspected endocrine disruptor on fetal steroidogenesis.

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Transfer and accumulation of cadmium, and the level of metallothionein in perfused human placentae

Cited by 49 publications

References 24 publications

Maternal, Placental and Cord Zinc Components in Healthy Women with Different Levels of Serum Zinc

Maternal, Placental and Cord Zinc Components in Healthy Women with Different Levels of Serum Zinc

Secretion of human chorionic gonadotropin in superfused young placental tissue exposed to cadmium

Effect of <i>in utero</i> exposure to endocrine disruptors on fetal steroidogenesis governed by the pituitary-gonad axis: a study in rats using different ways of administration

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