Increased dietary cadmium absorption in mice and human subjects with iron deficiency

Flanagan, Peter R.; McLellan, Julie; Haist, James V.; Cherian, M. George; Chamberlain, Michael J.; Valberg, L. S.

doi:10.1016/0016-5085(78)90138-5

Cited by 379 publications

(135 citation statements)

References 17 publications

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“…It has been suggested that the gastrointestinal absorption of Cd depends on the levels of iron in the body (Hamilton and Valberg 1974;Flanagan et al 1978), and this effect is associated with the divalent metal transported I (DMT1) (Park et al 2002). Since the gastrointestinal absorption of Cd is enhanced in iron-deficient animals, but reduced in iron-replete animals (Ryu et al 2004;Kim et al 2007).…”

Section: Discussionmentioning

confidence: 98%

Protective effect of ascorbic acid on cadmium-induced hypertension and vascular dysfunction in mice

et al. 2010

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Cadmium (Cd) is one of the most important environmental pollutants that cause a number of adverse health effects in humans and animals. Recent studies have shown that Cd-induced oxidative damage within the vascular tissues results in vascular dysfunction. The current study was aimed to investigate whether ascorbic acid could protect against Cd-induced vascular dysfunction in mice. Male ICR mice were received CdCl(2) (100 mg/l) via drinking water for 8 weeks alone or received ascorbic acid supplementation at doses of 50 and 100 mg/kg/day for every other day. Results showed that Cd administration increased arterial blood pressure and blunted the vascular responses to vasoactive agents. These alterations were related to increased superoxide production in thoracic aorta, increased urinary nitrate/nitrite, increased plasma protein carbonyl, elevated malondialdehyde (MDA) concentrations in plasma and tissues, decreased blood glutathione (GSH), and increased Cd contents in blood and tissues. Ascorbic acid dose-dependently normalized the blood pressure, improved vascular reactivities to acetylcholine (ACh), phenylephrine (Phe) and sodium nitroprusside (SNP). These improvements were associated with significant suppression of oxidant formation, prevention of GSH depletion, and partial reduction of Cd contents in blood and tissues. The findings in this study provide the first evidence in pharmacological effects of ascorbic acid on alleviation of oxidative damage and improvement of vascular function in a mouse model of Cd-induced hypertension and vascular dysfunction. Moreover, our study suggests that dietary supplementation of ascorbic acid may provide beneficial effects by reversing the oxidative stress and vascular dysfunction in Cd-induced toxicity.

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Section: Discussionmentioning

confidence: 98%

Protective effect of ascorbic acid on cadmium-induced hypertension and vascular dysfunction in mice

et al. 2010

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“…It has been demonstrated that the gastro-intestinal absorption of both Pb and Cd increases in women with depleted stores of iron, calcium and zinc (Vahter et al 2002). Moreover important bleedings associated to endometriosis may conceivably contribute to an additional depletion of the iron stores and, in turn, facilitate Cd or Pb absorption (Flanagan et al 1978;Goyer 1997).…”

Section: Discussionmentioning

confidence: 99%

Cadmium, lead and endometriosis

Heilier

Donnez

Verougstraete

et al. 2006

Int Arch Occup Environ Health

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“…Taken together these findings imply that intestinal cadmium uptake could be increased in a variety of disorders characterised by increased iron absorption (and therefore DMT1), including hereditary iron overload conditions. Interestingly, a study has shown increased blood cadmium levels in phlebotomised haemochromatosis patients (Akesson et al 2000), while others have shown increased blood cadmium (Barany et al 2005), or cadmium absorption (Flanagan et al 1978), in human iron deficiency. Previous studies in animals have focussed on the effect of dietary iron levels on cadmium absorption (Ragan 1977;Flanagan et al 1978;Park et al 2002).…”

Section: Introductionmentioning

confidence: 98%

Iron and cadmium uptake by duodenum of hypotransferrinaemic mice

2006

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Absorption from food is an important route for entry of the toxic metal, cadmium, into the body. Both cadmium and iron are believed to be taken up by duodenal enterocytes via the iron regulated, proton-coupled transporter, DMT1. This means that cadmium uptake could be enhanced in conditions where iron absorption is increased. We measured pH dependent uptake of (109)Cd and (59)Fe by duodenum from mice with an in vitro method. Mice with experimental (hypoxia, iron deficiency) or hereditary (hypotransferrinaemia) increased iron absorption were studied. All three groups of mice showed increased (59)Fe uptake (p<0.05) compared to their respective controls. Hypotransferrinaemic and iron deficient mice exhibited an increase in (109)Cd uptake (p<0.05). Cadmium uptake was not, however, increased by lowering the medium pH from 7.4 to 6. In contrast, (59)Fe uptake (from (59)FeNTA(2)) and ferric reductase activity was increased by lowering medium pH in control and iron deficient mice (p<0.05). The data show that duodenal cadmium uptake can be increased by hereditary iron overload conditions. The uptake is not, however, altered by lowering medium pH suggesting that DMT1-independent uptake pathways may operate.

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Increased dietary cadmium absorption in mice and human subjects with iron deficiency

Cited by 379 publications

References 17 publications

Protective effect of ascorbic acid on cadmium-induced hypertension and vascular dysfunction in mice

Protective effect of ascorbic acid on cadmium-induced hypertension and vascular dysfunction in mice

Cadmium, lead and endometriosis

Iron and cadmium uptake by duodenum of hypotransferrinaemic mice

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