Accumulation of cadmium in human placenta interacts with the transport of micronutrients to the fetus

Kippler, Maria; Hoque, A. M. Waheedul; Raqib, Rubhana; Öhrvik, Helena; Ekström, Eva‐Charlotte; Vahter, Marie

doi:10.1016/j.toxlet.2009.10.018

Cited by 199 publications

(151 citation statements)

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“…Indeed, the observed decrease of Zn contents in fetal liver and testis, measured in the present study, could be caused by Cd altered maternal Zn metabolism causing less transfer of this elements through the maternal side of placenta to the fetus by the inhibition of transport proteins [30,31]. Also, our results show that Cd was accumulated in the placenta and in fetal liver but it was not detected in the fetal testis of Cd exposed-animals.…”

Section: Discussionsupporting

confidence: 46%

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Chemek

Mimouna

Boughammoura

et al. 2016

Reproductive Toxicology

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Highlights Effects of Cd and Zn on testicular development were assessed. Cd accumulation and Zn depletion in testis during lactation were noted. Cd-induced abnormal seminiferous tubules and a plasmatic testosterone decrease. Zn supply induced a significant protection against Cd toxicity. Cd toxicity observed in pups is mediated by disruption of maternal Zn metabolism. *Research Highlights AbstractTo assess the effects of exposure to Cd and Zn on rat testicular development, offspring, from mothers receiving either tap water, Cd, Zn or Cd+Zn during gestation and lactation periods, were observed on gestational day (GD) 20 and on postnatal days (PND) 12, 21 and 35. During gestation, Cd induced maternal hypozincemia and less transfer of Zn to the fetus. During lactation, progressive Cd accumulation and Zn depletion in testis at PND12 and PND21 werenoted. An increase of abnormal seminiferous tubules and a decrease in testis weight and plasmatic testosterone concentration were also observed at PND21 and PND35 respectively. Interestingly, Zn supply induced a significant protection against Cd toxicity. These results suggest that the toxic effects of Cd observed during development are mediated by the disruption of Zn metabolism, which is established in mothers during pregnancy causing Zn deficiency in fetuses and continues to become more pronounced during lactation.

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Section: Discussionsupporting

confidence: 46%

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Chemek

Mimouna

Boughammoura

et al. 2016

Reproductive Toxicology

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“…The observation that anti-oxidants, i.e., α-lipoic acid and selenium, can alleviate a Cdproduced attenuation in the expression of testicular StAR supports the above view (El-Maraghy and Nassar, 2011). Cd is known to suppress the delivery of Zn to the fetus (Kuriwaki et al, 2005;Kippler et al, 2010). Because Zn defi ciency leads to a reduction in testicular steroidogenesis (Hamdi et al, 1997), an alternative possibility is that Cd suppresses the fetal production of sex steroids by lowering the Zn level.…”

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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“…It has been reported that maternal exposure to Cd negatively regulates birth weight, head, and chest circumference in females (18). One primary mechanism may be related to the elevated Cd concentration in the placenta, originating from increased maternal exposure (19), as a result of which Cd concentration in umbilical cord blood was increased and transferred to the fetus (20). Insufficient zinc level in fetus can cause intrauterine growth retardation (21).…”

Section: Discussionmentioning

confidence: 99%

Levels of Urine Cadmium in Children from Non-Polluted Areas of China

Zhao

2017

Iran J Pediatr

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Objectives: The database on cadmium (Cd) concentration in children is limited, especially in China. The present study aimed at evaluating the body burden of Cd and to propose reference values for urine Cd in young children, who lived in areas with no point sources of metal exposure. Methods: Overall, 1170 children aged from 1 month to 17 years old were enrolled in the study. A questionnaire was used to obtain essential information about age, gender, etc. Urine samples were collected to determine urinary Cd and urine creatinine. Results: A total of 1070 children, 544 males and 526 females, were included in the analysis. Based upon their age, the population was divided to three age groups (0 to 5 years, 6 to 11 years, and 12 to 17 years). The reference value of urinary Cd for children without disease and Cd exposure was as follows: 0 to 5 years < 0.56 µg/L, 6 to 11 years < 0.65 µg/L, and 12 to 17 years < 0.74 µg/L. The reference value of urinary Cd adjusted by urine specific gravity was as follows: 0 to 5 years < 0.83 µg/L, 6 to 11 years < 0.01 µg/L, and 12 to 17 years < 1.15 µg/L. The reference value of urinary Cd corrected by urinary creatinine was as follows: 0 to 5 years < 2.17 µg/L, 6 to 11 years < 1.23 µg/L, and 12 to 17 years < 1.25 µg/L. Conclusions:In this study, we determined urine cadmium levels in children from non-polluted areas in china. The reference intervals could be used to offer recommendations for clinical work.

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Accumulation of cadmium in human placenta interacts with the transport of micronutrients to the fetus

Cited by 199 publications

References 50 publications

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

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

Levels of Urine Cadmium in Children from Non-Polluted Areas of China

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