Expression of ZnT-1 (Slc30a1) and MT-1 (Mt1) in the conceptus of cadmium treated mice

Fernández, Estíbaliz L.; Dencker, Lennart; Tallkvist, Jonas

doi:10.1016/j.reprotox.2007.06.006

Cited by 16 publications

(10 citation statements)

References 28 publications

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“…Also Brambila et al (2002) failed to see induction of MT in the kidney of 1, 7, 14 and 21-day-old rats exposed to Hg8 vapor in utero. Cherian et al (1987) noted induction of MT by ZnSO 4 , but not by CdCl 2 in newborn rats' liver, while Fernandez et al (2007) measured an up-regulation of MT-1 gene expression in the mice embryo after single CdCl 2 injection to mice mothers.…”

Section: Introductionmentioning

confidence: 99%

Metallothionein, essential elements and lipid peroxidation in mercury-exposed suckling rats pretreated with selenium

et al. 2015

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Detoxification of mercury (Hg) with selenium (Se) in the early postnatal period with regard to the expression of metallothionein protein (MT), essential element status, and lipid peroxidation level in tissues has not been studied. Seven-day-old Wistar pups were orally pretreated with Se [6 μmol Na2SeO3/kg body weight (b.w.)] for 3 days and then cotreated with Hg (6 μmol HgCl2/kg b.w.) for the following 4 days. This group (Se + Hg) was compared to the groups treated with Hg, Se, or vehicle (control). Compared to the Hg-group, Se + Hg-group exhibited lower renal MT expression, reduced accumulation of Hg, Cu and Zn, and reduced excretion of Se, Hg and Zn in urine. In the liver, MT was stimulated by Se treatment in both, Se and Se + Hg-group. Hepatic and brain levels of the endogenous essential elements Cu, Fe, Mg, and Zn remained unchanged in all of the studied groups. Brain Hg levels and oxidation of lipids measured as thiobarbituric acid reactive substances were diminished in Se + Hg-group of pups compared to the Hg-group. This study suggests that Se pretreatment can help reduce Hg in the tissues of suckling rats, simultaneously preventing impairment of essential element levels in the kidneys and their excessive excretion via urine. Also, Se was shown to prevent oxidative damage of lipids in the brain, which is particularly susceptible to Hg during the early postnatal period.

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Section: Introductionmentioning

confidence: 99%

Metallothionein, essential elements and lipid peroxidation in mercury-exposed suckling rats pretreated with selenium

et al. 2015

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“…However, it has been shown that Zn transporter expression can be regulated by both transcriptional and post-transcriptional mechanisms in response to Zn availability to ensure an appropriate plasma concentration of this nutrient [3]. Zn transporters have been strongly implicated in embryonic, fetal, and neonatal development [2][3][4][5]. SLC30A1 and SLC30A5 play a key role in regulating delivery of maternal Zn to the developing embryo [2,5].…”

Section: Introductionmentioning

confidence: 99%

“…Zn transporters have been strongly implicated in embryonic, fetal, and neonatal development [2][3][4][5]. SLC30A1 and SLC30A5 play a key role in regulating delivery of maternal Zn to the developing embryo [2,5]. Cadmium exposure, which is known to be risk factor for congenital anomalies, down-regulates Slc30a1 expression, indicating that maternal cadmium exposure may alter Zn homeostasis in the conceptus [5].…”

Section: Introductionmentioning

confidence: 99%

“…SLC30A1 and SLC30A5 play a key role in regulating delivery of maternal Zn to the developing embryo [2,5]. Cadmium exposure, which is known to be risk factor for congenital anomalies, down-regulates Slc30a1 expression, indicating that maternal cadmium exposure may alter Zn homeostasis in the conceptus [5]. Mutations in ZnTs and ZIPs reveal their physiological functions [3].…”

Section: Introductionmentioning

confidence: 99%

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Lack of association of polymorphic variants of genes encoding zinc transporters with the risk of orofacial cleft-affected pregnancies.

Hozyasz

Mostowska²,

Lianeri³

et al. 2011

Folia Histochem Cytobiol.

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Maternal zinc deficiency seems to be a risk factor for orofacial clefts in offspring. This study was undertaken to investigate the involvement of polymorphic variants of genes for zinc transporters in the susceptibility of clefting. PCR-RFLP analysis was used to analyze single nucleotide polymorphisms of SLC30A1 (rs7526700, rs2278651, rs611386), SLC30A4 (rs2453531, rs8029246), SLC30A5 (rs351444, rs164393, rs6886492), SLC39A1 (rs10127484, rs11264736), and SLC39A3 (rs759071, rs4806874, rs10415622) in mothers of children with non-syndromic cleft lip with or without cleft palate (CL/P) and control mothers. The allele, genotype, and haplotype distribution was found to be similar among case and control mothers. Also, the gene-by-gene interaction analysis conducted using the Multifactor Dimensionality Reduction approach revealed no significant interactive genetic effect on having a child with a cleft. In conclusion, our results demonstrated that the analyzed polymorphic variants of genes for zinc transporters are not implicated in abnormal palatogenesis in the investigated group of women from the Polish population.

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“…Based on these observations, several biomarkers of response have been proposed for use with Cd, including established markers associated with alterations in metal ion regulation, such as metallothioneins (e.g. Mt1 and Mt2) characterized in their involvement in Cd sequesteration [16, 17] and specific divalent ion transporters (ex. DMT1) which regulate Cd cellular uptake [18].…”

Section: Introductionmentioning

confidence: 99%

Embryonic toxicokinetic and dynamic differences underlying strain sensitivity to cadmium during neurulation

Robinson

Hong

et al. 2010

Reproductive Toxicology

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Differences in sensitivity are observed between mouse strains, C57 (sensitive) and SWV (resistant) when exposed to cadmium (Cd) during the neurulation period. In this study, we investigated the toxicokinetics of Cd in relation with toxicodynamic responses to identify factors affecting differential Cd-sensitivity in C57 and SWV. Using a level of exposure which induced developmental toxicity and differential effects between strains, we assessed maternal and embryonic Cd uptake and evaluated biomarkers of response previously linked with Cd exposure, specifically metal ion regulators (Mt1, Mt2, DMT1) and markers of cell cycle arrest/apoptosis induction (p53, Cdkn1a, c-Casp3). Greater Cd uptake was observed in C57 embryos compared to SWV and these observations of differential uptake were associated with increased alterations in expression of biomarkers of metal response (e.g. c-Casp3) and strain sensitivity. Using sensitive and resistant mouse strains, we have identified toxicokinetic and dynamic differences which underlie observed differences in Cd-embryonic sensitivity and response.

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Expression of ZnT-1 (Slc30a1) and MT-1 (Mt1) in the conceptus of cadmium treated mice

Cited by 16 publications

References 28 publications

Metallothionein, essential elements and lipid peroxidation in mercury-exposed suckling rats pretreated with selenium

Metallothionein, essential elements and lipid peroxidation in mercury-exposed suckling rats pretreated with selenium

Lack of association of polymorphic variants of genes encoding zinc transporters with the risk of orofacial cleft-affected pregnancies.

Embryonic toxicokinetic and dynamic differences underlying strain sensitivity to cadmium during neurulation

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