Evaluation of the effect of divalent metal transporter 1 gene polymorphism on blood iron, lead and cadmium levels

Kayaaltı, Zeliha; Akyüzlü, Dilek Kaya; Söylemezoğlu, Tülın

doi:10.1016/j.envres.2014.11.008

Cited by 41 publications

(15 citation statements)

References 46 publications

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“…The transport process of heavy metals is regulated by specific transporters. Divalent metal transporter 1 (DMT1), known as natural resistance-associated macrophage protein 2 (NRAMP2), divalent cation transporter 1 (DCT1), or solute carrier family 11, member 2 (SLC11A2), is a divalent metal transporter belonging to the proton-coupled metal-ion transporter family ( 160 , 161 ). It regulates the transportation of bivalent metals including Fe, Zn, Mn, Cu, Co, Ni, Cd, and Pb ( 160 ).…”

Section: Discussionmentioning

confidence: 99%

Relationships Between Biological Heavy Metals and Breast Cancer: A Systematic Review and Meta-Analysis

et al. 2022

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IntroductionHeavy metals were classified as essential, probably essential, and potentially toxic in the general population. Until now, it has been reported inconsistently on the association between heavy metals and BC. In this meta-analysis, we aimed to assess the association between heavy metals and BC and review the potential mechanisms systematically.MethodsWe searched for epidemiological studies in English about the association between heavy metals and BC published before September 2020 in PubMed, Web of Science, and Embase databases. In total 36 studies, comprising 4,151 individuals from five continents around the world were identified and included.ResultsIn all biological specimens, Cu, Cd, and Pb concentrations were higher, but Zn and Mn concentrations were lower in patients with BC than in non-BC participants [SMD (95% CIs): 0.62 (0.12, 1.12); 1.64 (0.76, 2.52); 2.03 (0.11, 3.95); −1.40 (−1.96, −0.85); −2.26 (−3.39, −1.13); p = 0.01, 0.0003, 0.04, <0.0001, <0.0001]. Specifically, higher plasma or serum Cu and Cd, as well as lower Zn and Mn, were found in cases [SMD (95% CIs): 0.98 (0.36, 1.60); 2.55 (1.16, 3.94); −1.53 (−2.28, −0.78); −2.40 (−3.69, −1.10); p = 0.002, 0.0003, <0.0001, 0.0003]; in hair, only lower Zn was observed [SMD (95% CIs): −2.12 (−3.55, −0.68); p = 0.0004]. Furthermore, the status of trace elements probably needs to be re-explored, particularly in BC. More prospective studies, randomized clinical trials, and specific pathogenic studies are needed to prevent BC. The main mechanisms underlying above-mentioned findings are comprehensively reviewed.ConclusionFor BC, this review identified the current knowledge gaps which we currently have in understanding the impact of different heavy metals on BC.Systematic Review Registrationwww.crd.york.ac.uk/prospero/display_record.php?ID=CRD42020176934, identifier: CRD42020176934.

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Section: Discussionmentioning

confidence: 99%

Relationships Between Biological Heavy Metals and Breast Cancer: A Systematic Review and Meta-Analysis

et al. 2022

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“…The divalent metal transporter 1 (DMT1; encoded by the SLC11a2 gene which is polymorphic (Kayaalti et al., 2015)) mediates the transport of nickel and other divalent metal ions such as iron from the lumen of the intestine into the enterocyte and export of iron from endocytic vesicles. DMT1 also mediates apical uptake of divalent cations in the kidney, and has been shown to be involved in recovery of iron from recycling endosomes during transferrin receptor‐associated cellular uptake in various cell types (Mackenzie and Garrick, 2005).…”

Section: Assessmentmentioning

confidence: 99%

Update of the risk assessment of nickel in food and drinking water

Schrenk¹,

Bignami²,

Bodin³

et al. 2020

EFS2

101

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The European Commission asked EFSA to update its previous Opinion on nickel in food and drinking water, taking into account new occurrence data, the updated benchmark dose (BMD) Guidance and newly available scientific information. More than 47,000 analytical results on the occurrence of nickel were used for calculating chronic and acute dietary exposure. An increased incidence of postimplantation loss in rats was identified as the critical effect for the risk characterisation of chronic oral exposure and a BMDL 10 of 1.3 mg Ni/kg body weight (bw) per day was selected as the reference point for the establishment of a tolerable daily intake (TDI) of 13 lg/kg bw. Eczematous flare-up reactions in the skin elicited in nickel-sensitised humans, a condition known as systemic contact dermatitis, was identified as the critical effect for the risk characterisation of acute oral exposure. A BMDL could not be derived, and therefore, the lowest-observed-adverse-effect-level of 4.3 lg Ni/kg bw was selected as the reference point. The margin of exposure (MOE) approach was applied and an MOE of 30 or higher was considered as being indicative of a low health concern. The mean lower bound (LB)/upper bound (UB) chronic dietary exposure was below or at the level of the TDI. The 95th percentile LB/UB chronic dietary exposure was below the TDI in adolescents and in all adult age groups, but generally exceeded the TDI in toddlers and in other children, as well as in infants in some surveys. This may raise a health concern in these young age groups. The MOE values for the mean UB acute dietary exposure and for the 95th percentile UB raises a health concern for nickel-sensitised individuals. The MOE values for an acute scenario regarding consumption of a glass of water on an empty stomach do not raise a health concern.

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“…In humans, a range factors are known to influence uptake of chemicals from the gut into blood circulation. These include mucus production [42] and polymorphisms in genes for transport proteins such as divalent metal transporter 1 (for metals) [43] and multidrug resistance protein 1 (MDR1; for pharmaceuticals) [44]. In humans, gut microbial community composition also influences xenobiotic metabolism [45] and can be influenced by host genotype [46].…”

Section: Physiological Mechanisms For Adaptations and Their Potentialmentioning

confidence: 99%

Adaptive capabilities and fitness consequences associated with pollution exposure in fish

Hamilton

Rolshausen

Webster

et al. 2017

Phil. Trans. R. Soc. B

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Many fish populations are exposed to harmful levels of chemical pollution and selection pressures associated with these exposures have led to the evolution of tolerance. Our understanding of the physiological basis for these adaptations is limited, but they are likely to include processes involved with the absorption, distribution, metabolism and/or excretion of the target chemical. Other potential adaptive mechanisms include enhancements in antioxidant responses, an increased capacity for DNA and/or tissue repair and alterations to the life cycle of fish that enable earlier reproduction. Analysis of single-nucleotide polymorphism frequencies has shown that tolerance to hydrocarbon pollutants in both marine and estuarine fish species involves alteration in the expression of the xenobiotic metabolism enzyme CYP1A. In this review, we present novel data showing also that variants of the CYP1A gene have been under selection in guppies living in Trinidadian rivers heavily polluted with crude oil. Potential costs associated with these adaptations could reduce fitness in unpolluted water conditions. Integrating knowledge of local adaptation to pollution is an important future consideration in conservation practices such as for successful restocking, and improving connectivity within river systems.This article is part of the themed issue ‘Human influences on evolution, and the ecological and societal consequences’.

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Evaluation of the effect of divalent metal transporter 1 gene polymorphism on blood iron, lead and cadmium levels

Cited by 41 publications

References 46 publications

Relationships Between Biological Heavy Metals and Breast Cancer: A Systematic Review and Meta-Analysis

Relationships Between Biological Heavy Metals and Breast Cancer: A Systematic Review and Meta-Analysis

Update of the risk assessment of nickel in food and drinking water

Adaptive capabilities and fitness consequences associated with pollution exposure in fish

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