Does maternal VDR FokI single nucleotide polymorphism have an effect on lead levels of placenta, maternal and cord bloods?

Kaya-Akyüzlü, Dilek; Kayaaltı, Zeliha; Koca, Deniz; Söylemezoğlu, Tülın

doi:10.1016/j.placenta.2015.06.012

Cited by 9 publications

(3 citation statements)

References 42 publications

(64 reference statements)

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“…(11,20,21). However different results could be reported in some studies, due to the variety of exposure matrices, dietary patterns, environmental factors, and genetic predisposition (11,25,26).…”

Section: Discussionmentioning

confidence: 97%

Assessment of lead and mercury levels in maternal blood, fetal cord blood and placenta in pregnancy with intrauterine growth restriction

Yüksel

Kalafat

Katlan

et al. 2022

Journal of Basic and Clinical Health Sciences

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Purpose: Many studies reported that prenatal exposure to lead and mercury are correlated with reduced birth weight and size, and these metals can cause adverse effects on neurodevelopment. In this study, it was aimed to investigate and compare the lead and mercury levels in maternal blood, cord blood, and placenta in pregnant women with IUGR fetuses diagnosed using abnormal Doppler findings and pregnant women with healthy fetuses. Material and Methods: This study included 75 patients, comprising 41 in IUGR group and 34 in control group. Maternal venous blood, fetal cord blood and placental samples were taken during delivery period. Results: Mercury levels in maternal blood and fetal cord blood, and lead levels in the placenta were found to be significantly higher in the IUGR group than in healthy subjects. Correlation analysis revealed that measurement values of body weight, body height, and head circumference of fetus might be lower when mercury level was measured higher in maternal blood and fetal cord blood. Furthermore, fetal body weight and fetal body height also would be lower when lead level measured in placenta was higher. Logistic Regression analysis results revealed that mercury levels measured in fetal cord blood could be used as the best marker in predicting low fetal weight, low fetal body height, and low fetal head circumference. Conclusion:In conclusion, it was thought with this study results that in order to identify the etiology and to give therapeutic prenatal care of the IUGR in a fetus diagnosed as idiopathic IUGR it would be appropriate to measure the level of lead and especially mercury in the fetal cord blood during the prenatal follow-up period.

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Section: Discussionmentioning

confidence: 97%

Assessment of lead and mercury levels in maternal blood, fetal cord blood and placenta in pregnancy with intrauterine growth restriction

Yüksel

Kalafat

Katlan

et al. 2022

Journal of Basic and Clinical Health Sciences

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“…VDR level is also thought to be a determinant of cellular responsiveness to VD [ 61 ]. The VDR gene polymorphism has been found to increase or decrease human susceptibility to Pb poisoning [ 62 ] and different VDR genotypes have been associated with different Pb-induced toxic effects [ 62 , 63 , 64 , 65 , 66 , 67 ]. Immunohistochemical results have shown that the VDR expression was restricted to the nucleus and localized mainly to brain cortex and thalamus ( Figure 9 and Figure 10 ) and these results are in agreement with previously reported data [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

Lead Affects Vitamin D Metabolism in Rats

2018

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A negative association between blood lead and vitamin D concentrations has been reported, however, experimental data on the effect of lead (Pb) on vitamin D metabolism is scarce. We investigated the effects of Pb on serum vitamin D metabolites, vitamin D activating enzymes and vitamin D receptor (VDR) in rats. Newborn Wistar rat pups were exposed to 0.2% Pb-acetate via their dams’ drinking water from post-natal day (PND) 1 to 21 and directly in drinking water until PND30. Serum 25-hydroxyvitamin D was analyzed with LC-MS/MS and 1,25-dihydroxyvitamin D with an immunoassay. Tissue expression of vitamin D activating enzymes and VDR were measured by Western blot and immunohistochemistry. Serum 25-hydroxyvitamin D was significantly decreased at both PND21 and PND30, whereas 1,25-dihydroxyvitamin D was decreased (p < 0.05) only at PND21 in the Pb-exposed rats. Expression of renal 1-α-hydroxylase was decreased by Pb only at PND21 (p < 0.05) but the brain 1-α-hydroxylase was not affected. Hepatic 25-hydroxylase expression was significantly decreased at PND21 but significantly increased at PND30 by Pb exposure. VDR expression in the brain was increased at both PND21 and PND30 (p < 0.05). These results suggest that Pb interferes with vitamin D metabolism by affecting the expression of its metabolizing enzymes.

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“…Consequently, a relatively higher transmission is reported for Pb across the placental membrane (Goyer, 1990). A 1% Pb increase in maternal blood was shown to increase placental Pb by 0.43% (Kaya-Akyüzlü et al, 2015). Cord blood Pb levels are considered the primary bioindicator for fetal exposure at the prenatal stage (Reichrtová et al, 1998).…”

Section: Mechanisms Of Placental Membrane Crossing By Pbmentioning

confidence: 99%

On‐going consequences of in utero exposure of Pb: An epigenetic perspective

Tasin

Ahmed

Halder

et al. 2022

J of Applied Toxicology

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Epigenetic modifications by toxic heavy metals are one of the intensively investigated fields of modern genomic research. Among a diverse group of heavy metals, lead (Pb) is an extensively distributed toxicant causing an immense number of abnormalities in the developing fetus via a wide variety of epigenetic changes. As a divalent cation, Pb can readily cross the placental membrane and the fetal blood brain barrier leading to far-reaching alterations in DNA methylation patterns, histone protein modifications, and micro-RNA expression. Over recent years, several human cohorts and animal model studies have documented hypermethylation and hypomethylation of developmental genes along with altered DNA methyl-transferase expression by in utero Pb exposure in a dose-, duration-, and sex-dependent manner. Modifications in the expression of specific histone acetyltransferase enzymes along with histone acetylation and methylation levels have been reported in rodent and murine models.Apart from these, down-regulation and up-regulation of certain microRNAs crucial for fetal development have been shown to be associated with in utero Pb exposure in human placenta samples. All these modifications in the developing fetus during the prenatal and perinatal stages reportedly caused severe abnormalities in early or adult age, such as impaired growth, obesity, autism, diabetes, cardiovascular diseases, risks of cancer development, and Alzheimer's disease. In this review, currently available information on Pb-mediated alterations in the fetal epigenome is summarized. Further research on Pb-induced epigenome modification will help to understand the mechanisms in detail and will enable us to formulate safety guidelines for pregnant women and developing children.

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Does maternal VDR FokI single nucleotide polymorphism have an effect on lead levels of placenta, maternal and cord bloods?

Cited by 9 publications

References 42 publications

Assessment of lead and mercury levels in maternal blood, fetal cord blood and placenta in pregnancy with intrauterine growth restriction

Assessment of lead and mercury levels in maternal blood, fetal cord blood and placenta in pregnancy with intrauterine growth restriction

Lead Affects Vitamin D Metabolism in Rats

On‐going consequences of in utero exposure of Pb: An epigenetic perspective

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