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Dietary Strategies for the Treatment of Cadmium and Lead Toxicity - 02 Essential metals

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This is such a good paper, so clear, well written and helpful that I have included it in full

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Nutrients. 2015 Jan; 7(1): 552–571.  Published online 2014 Jan 14. doi:  10.3390/nu7010552 PMCID: PMC4303853  Dietary Strategies for the Treatment of Cadmium and Lead Toxicity - Qixiao Zhai,1 Arjan Narbad,2 and Wei Chen1,3,*

2. Essential Metals

Many studies in both animals and humans have shown that a deficiency in essential metals such as zinc, calcium  or iron  can lead to greater absorption and toxicity of Cd and Pb. Therefore it is logical to suggest that the supplementation with essential metals can provide protective effects against Cd and Pb intoxication. A selection of such studies listed in Table 1 show the benefits of essential metals in this context.

 Zinc is one of the most well studied essential metals for the alleviation of heavy metal toxicity. As zinc has similar chemical and physical properties to Cd and Pb, it competes for the binding sites of metal absorptive and enzymatic proteins . Intake of zinc also induces the synthesis of metallothionein (MT), a low molecular weight protein that has a high affinity for Cd and causes detoxification by binding Cd. Zinc supplementation effectively protects the activity of blood δ-aminolevulinic acid dehydratase (ALAD), a zinc-dependent enzyme that is very sensitive to Pb toxicity. Moreover, zinc intake has been reported to alleviate the oxidative stress caused by Cd and Pb exposure, which may be due to zinc’s functionality as a cofactor of the antioxidant enzyme copper zinc-superoxide dismutase (Cu/Zn SOD).

A considerable number of studies have shown that selenium administration is protective against Cd and Pb toxicity within a range of different organs of mice including the brain, lungs, liver, kidneys and blood. Selenium is a cofactor of the antioxidant enzyme glutathione peroxidase (GPx) and it contributes to the antioxidant defence system, which enables it to alleviate Cd and Pb toxicity by reducing the Cd/Pb-induced oxidative stress and enhancing the antioxidant capacity of the host. It is also believed that selenium may form inactive complexes with heavy metals which can further enhance their detoxification.

Iron competes with Cd for access to intestinal metal uptake transporters including divalent metal transporter-1 (DMT1) and metal transporter protein 1 (MTP1), which may explain the decrease in intestinal Cd absorption after iron supplementation. Moreover, the expression of these transporters is often modulated by nutritional status of essential minerals such as iron and zinc. For instance iron deficiency has been reported to up-regulate the expression of DMT1 in intestinal epithelium. Hence iron supplement can prevent or limit Cd absorption by reducing the expression of such transporters. On the other hand, as iron is a component of the heme complex, the deficiency of iron will enhance Pb toxicity to the heme synthesis system .

Other essential metals, such as calcium and magnesium, have also been reported to be effective against Cd and Pb toxicity (Table 1). These essential metals can reduce the heavy metal burden by competing with Pb or Cd for intestinal absorption and prevent heavy metal induced tissue damage by competitive binding to active sites of the enzymes.

In summary, these essential metals decrease intestinal Cd and Pb absorption, recover the essential metal homeostasis and alleviate the oxidative stress caused by Cd and Pb toxicity.

Diet associated essential metal supplementation should be regarded as important for essential metal-deficient people, such as children and pregnant women. Because without sufficient essential metal stores to prevent heavy metal absorption, these people are especially susceptible to heavy metal toxicity. It should also be noted that Cd and Pb exposure cause the loss of essential metals, which leads to complications such as iron-deficiency anaemia and osteoporosis. Appropriate concentrations of essential metal supplementation is therefore also beneficial for preventing these complications.

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References

Table 1

Selected studies on the protective effects of essential metals against Cd and Pb toxicity.

Essential MetalAdministered FormDurationAnimalModelTargetSitesProtectiveEffectsRef.
Zinc 40 mg/L ZnCl2 in drinking water 30 days Male rats exposed to 40 mg/L CdCl2 in drinking water Testes Zinc restored the activity of GPx and SOD in the testes and attenuated DNA oxidation in the gonads. [40]
0.02% Zn2+ in drinking water PND 1 to PND 21, stop at weaning Pregnant mice exposed to 0.2% Pb-acetate in drinking water Brain Zinc restored the activity of SOD, XO and CAT, and decreased the LP levels in the pups’ brains. [41]
Selenium 20 μmol/kg b.w. (PhSe)2 by oral treatment 4 weeks Male rats exposed to 10 μmol/kg b.w. CdCl2 (s.c.) Brain and lungs (PhSe)2 restored the activity of SOD and CAT, increased the vitamin C content and decreased the level of LP in the brain. It also decreased the Cd level in the lungs. [42]
  0.2 mg/L Na2SeO3 in drinking water 21 days Lactating rats exposed to 100 mg/L Pb-acetate in drinking water Brain and nervous system Na2SeO3 improved the spatial memory and the level of LTP and decreased neuron apoptosis in the pups. [43]
Iron 120 mg/kg b.w. Fe in diet 4 or 8 weeks Male rats exposed to 100 μg/kg b.w. CdCl2 by oral gavage Kidney, liver and intestinal tract An iron-sufficient diet decreased the Cd burden in the tissue and regulated intestinal Cd absorption through the iron transporters. [45]
Calcium 0.02% Ca2+ in drinking water GD 6 to PND 21 Pregnant mice exposed to 0.2% Pb-acetate in drinking water Brain and nervous system Calcium decreased the synaptosomal AChE and mitochondrial MAO activity and improved the pups’ total locomotor activity and exploratory behaviour. [48]
Magnesium 20 mg/kg b.w. Mg orally 1 or 2 weeks Male mice exposed to 10 mg/kg b.w. Cd Testes and kidneys Mg pre-treatment was efficient in restoring the renal and testis GSH levels. [49]

AChE, acetylcholinesterase; b.w., body weight; CAT, catalase; GD, gestational day; GPx, glutathione peroxidase; GSH, glutathione; LTP, hippocampal long-term potentiation; LP, lipid peroxidation; MAO, monoamine oxidase; PND, postnatal day; s.c., subcutaneously; SOD, superoxide dismutase; XO, xanthine oxidase.