Iron retention and distribution in the cadmium-induced iron deficiency

Schäfer, S. G.; Elsenhans, Bernd

doi:10.1016/0147-6513(85)90014-4

Cited by 21 publications

(5 citation statements)

References 25 publications

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“…Cadmium loading decreases heart, lung, spleen, muscle, and femur iron concentrations in rats R. norvegicusas by means of inhibiting intestinal iron absorption in a competitive manner, probably because the two metals share one or more steps in the absorptive process (Hamilton and Valberg, 1974;Schäfer and Elsenhans, 1985;Pond and Walker, 1975;Crowe and Morgan, 1997). In the present study, iron concentrations in kidney and liver were detected and showed a notable decreased trend with the increase of dietary Cd level.…”

Section: Cadmium Iron and Calcium Accumulations In Different Tissuesmentioning

confidence: 42%

Toxic effects of two sources of dietborne cadmium on the juvenile cobia, Rachycentron canadum L. and tissue-specific accumulation of related minerals

et al. 2015

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Section: Cadmium Iron and Calcium Accumulations In Different Tissuesmentioning

confidence: 42%

Toxic effects of two sources of dietborne cadmium on the juvenile cobia, Rachycentron canadum L. and tissue-specific accumulation of related minerals

et al. 2015

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“…Lower levels of body iron would likely result in increase in DMT1 expression in the intestine (2) because of the IRE located at the 3Ј-end of DMT1 mRNA. Hence, the competition between cadmium and iron provides a molecular mechanism to explain both the process of iron deficiency induced by chronic exposure to cadmium (12) and the increased absorption of dietary cadmium shown in humans who are iron deficient (26).…”

Section: Discussionmentioning

confidence: 99%

Effect of DMT1 knockdown on iron, cadmium, and lead uptake in Caco-2 cells

Bannon

Abounader

Lees

et al. 2003

American Journal of Physiology-Cell Physiology

202

119

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(divalent metal transporter 1) is a hydrogen-coupled divalent metal transporter with a substrate preference for iron, although the protein when expressed in frog oocytes transports a broad range of metals, including the toxic metals cadmium and lead. Wild-type Caco-2 cells displayed saturable transport of lead and iron that was stimulated by acid. Cadmium and manganese inhibited transport of iron, but zinc and lead did not. The involvement of DMT1 in the transport of toxic metals was examined by establishing clonal DMT1 knockdown and control Caco-2 cell lines. Knockdown cell lines displayed much lower levels of DMT1 mRNA and a smaller Vmax for iron uptake compared with control cell lines. One clone was further characterized and found to display an ϳ50% reduction in uptake of iron across a pH range from 5.5 to 7.4. Uptake for cadmium also decreased 50% across the same pH range, but uptake for lead did not. These results show that DMT1 is important in iron and cadmium transport in Caco-2 cells but that lead enters these cells through an independent hydrogen-driven mechanism.

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“…It has been reported that Cd treatment could cause an increase in iron content in the kidneys or testes [21,42,52,53]. Studies with contradictory results have reported that Cd reduces iron levels in the body, possibly involving a reduction in iron absorption by Cd through competitive binding to divalent metal cation transport receptors in the small intestine [19,54,55]. Previous studies have found that Cd, as a divalent metal cation, can interfere competitively with the absorption of other divalent metal ions, such as iron, copper, and manganese, through divalent metal cation channels in the digestive tract (especially in the small intestine), causing essential trace element deficiency diseases such as anemia [22,23].…”

Section: Discussionmentioning

confidence: 99%

Cadmium Induces Kidney Iron Deficiency and Chronic Kidney Injury by Interfering with the Iron Metabolism in Rats

Zhang,

Long,

Dong

et al. 2024

IJMS

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Cadmium (Cd) is a common environmental pollutant and occupational toxicant that seriously affects various mammalian organs, especially the kidney. Iron ion is an essential trace element in the body, and the disorder of iron metabolism is involved in the development of multiple pathological processes. An iron overload can induce a new type of cell death, defined as ferroptosis. However, whether iron metabolism is abnormal in Cd-induced nephrotoxicity and the role of ferroptosis in Cd-induced nephrotoxicity need to be further elucidated. Sprague Dawley male rats were randomly assigned into three groups: a control group, a 50 mg/L CdCl2-treated group, and a 75 mg/L CdCl2-treated group by drinking water for 1 month and 6 months, respectively. The results showed that Cd could induce renal histopathological abnormalities and dysfunction, disrupt the mitochondria’s ultrastructure, and increase the ROS and MDA content. Next, Cd exposure caused GSH/GPX4 axis blockade, increased FTH1 and COX2 expression, decreased ACSL4 expression, and significantly decreased the iron content in proximal tubular cells or kidney tissues. Further study showed that the expression of iron absorption-related genes SLC11A2, CUBN, LRP2, SLC39A14, and SLC39A8 decreased in proximal tubular cells or kidneys after Cd exposure, while TFRC and iron export-related gene SLC40A1 did not change significantly. Moreover, Cd exposure increased SLC11A2 gene expression and decreased SLC40A1 gene expression in the duodenum. Finally, NAC or Fer-1 partially alleviated Cd-induced proximal tubular cell damage, while DFO and Erastin further aggravated Cd-induced cell damage. In conclusion, our results indicated that Cd could cause iron deficiency and chronic kidney injury by interfering with the iron metabolism rather than typical ferroptosis. Our findings suggest that an abnormal iron metabolism may contribute to Cd-induced nephrotoxicity, providing a novel approach to preventing kidney disease in clinical practice.

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Iron retention and distribution in the cadmium-induced iron deficiency

Cited by 21 publications

References 25 publications

Toxic effects of two sources of dietborne cadmium on the juvenile cobia, Rachycentron canadum L. and tissue-specific accumulation of related minerals

Toxic effects of two sources of dietborne cadmium on the juvenile cobia, Rachycentron canadum L. and tissue-specific accumulation of related minerals

Effect of DMT1 knockdown on iron, cadmium, and lead uptake in Caco-2 cells

Cadmium Induces Kidney Iron Deficiency and Chronic Kidney Injury by Interfering with the Iron Metabolism in Rats

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