Effects of subcutaneous and oral cadmium on iron metabolism: Role of ceruloplasmin and metallothionein

Sakata, Naoki; Sugawara, Chieko; Miyake, Hirotsugu

doi:10.1007/bf00316347

Cited by 23 publications

(2 citation statements)

References 21 publications

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“…Patients with itai-itai disease showed renal anemia, not iron deficiency (Horiguchi et al, 1994;Nogawa et al, 1984). In animals, increased iron concentration in organs was observed after long-term dietary Cd exposure (Stonard and Webb, 1976) or both acute and chronic parenteral Cd exposure (Maitani and Suzuki, 1986;Sugawara et al, 1984). These results suggest that Cd interferes with intestinal iron absorption to induce iron deficiency via oral exposure, but Cd highly accumulated in organs after parenteral or long-term oral exposure would induce excess iron accumulation, which could lead to EPO suppression.…”

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Cadmium Induces Anemia through Interdependent Progress of Hemolysis, Body Iron Accumulation, and Insufficient Erythropoietin Production in Rats

Horiguchi¹,

Oguma²,

Kayama³

2011

Toxicological Sciences

109

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Cadmium is a toxic heavy metal and distributed widely in the environment. In addition to damaging the liver, kidneys, and bone, cadmium causes anemia through hemolysis, iron deficiency, and insufficient erythropoietin (EPO) production (renal anemia) along with changes in iron metabolism. Here, we investigated the role of iron in the interdependent progress of three types of anemia in cadmium-injected rats fed iron-sufficient or iron-deficient diets for 1 or 3 months. Cadmium injections for 1 month induced renal anemia without renal injury. Injections for 3 months induced hemolysis, iron deficiency, and renal anemia, accompanied by hepatic and renal damage. Iron concentrations in the liver, kidney, and spleen were increased, derived from internally released iron from hemolyzed red blood cells, increased duodenal iron absorption, insufficient erythropoiesis, and hepatic ferritin overproduced by cadmium-induced interleukin-6. Therefore, the iron deficiency anemia was actually apparent. Cadmium suppressed renal EPO production through a direct effect, accumulated iron, and destruction of EPO-producing cells. Increased duodenal iron absorption could be attributed to hypertrophy of the duodenal mucosa derived from anemia. Thus, insufficient EPO production and iron accumulation are the central factors driving anemia in cadmium toxicity.

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confidence: 87%

Cadmium Induces Anemia through Interdependent Progress of Hemolysis, Body Iron Accumulation, and Insufficient Erythropoietin Production in Rats

Horiguchi¹,

Oguma²,

Kayama³

2011

Toxicological Sciences

109

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“…Cd'un karaciğer ve böbreklerde demir artışına neden olurken serum demir düzeyini alınan doz ve süre ile uygulama şekline bağlı olarak değiştirdiği bildirilmiştir (38 …”

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Kadmi̇yum Ve Etanolün Li̇pi̇d Peroksi̇dasyon, İz Element Düzeyleri̇ Ve Bi̇yoki̇myasal Göstergeler Üzeri̇ne Etki̇si̇ : Effects of Cadmium and Ethanol on Lipid Peroxidation, Trace Element Levels and Biochemical

Aktay¹,

Söylemezoğlu²

1998

Ankara Universitesi Eczacilik Fakultesi Dergisi

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Kadmiyum ve etanolün ayrı ayrı ve birlikte alındıklarında toksik etki mekanizmalarını araştırmak amacıyla karaciğerde malondialdehit; karaciğer, böbrek, kalp, ve serumda çinko, bakır ve demir içeriği ile serum alkalen fosfataz (ALP) ,glutamik okzalasetik transaminaz (GOT) ve glutamik pirüvik transaminaz (GPT) enzim düzeyleri çalışıldı. Karaciğerde malondialdehit düzeyleri tüm deney gruplarında kontrol grubuna göre anlamlı derecede yüksek bulundu. Kadmiyum (3 mg/kg, IP), maruziyeti tüm organlarda ve serumda çinko, karaciğer ve böbreklerde ise demir düzeyinde artışa neden oldu. Etanol (% 5-10 h/h) alımı karaciğer ve böbreklerde çinko düzeyini etkilemezken karaciğer, böbrek ve kalpte demir düzeyini anlamlı derecede artırdı. Diğer taraftan, deney gruplarının serum ALP, GOT ve GPT enzim düzeylerinde anlamlı artışlar gözlenirken doku ve serum bakır düzeylerinde anlamlı bir farklılık bulunmadı.

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Relationship between ceruloplasmin and Cu status involving metallothionein induced by several heavy metals in the mouse

Sakata

Sugawara

1987

Arch Toxicol

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ICR male mice aged 5 weeks were injected subcutaneously with CdCl2, Pb(CH3COO)2, AgNO3, CuCl2, a combination of Cd and Ag compounds, or a combination of Cu and Ag compounds. These injections were carried out 3 times. Twenty-four hours after the last injection, they were sacrificed. Cd injection significantly stimulated serum ceruloplasmin (Cp) activity and Cu concentration, accompanied by an increase in hepatic Cu. Pb injection also slightly increased the Cp level. In contrast, Ag injection markedly decreased both Cp activity and Cu concentration in the serum. Hepatic Cu increased slightly after Ag injection. Using a combination of Cd and Ag, only the Ag effect on the Cp activity appeared. The Cu injection stimulated Cu binding to metallothionein (MT) and bile excretion of Cu, but not Cp release. With a Cu and Ag combination, the effect of Ag on Cp was lost, with a concomitant disappearance of Ag from the Cp fraction in the serum. Our results suggest that in the mouse, Cd and Ag, Cu antagonistic metals, influence different sites of Cp metabolism. Excess hepatic Cu is partly eliminated by excretion of bile and is partly detoxified by MT induction.

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Effects of subcutaneous and oral cadmium on iron metabolism: Role of ceruloplasmin and metallothionein

Cited by 23 publications

References 21 publications

Cadmium Induces Anemia through Interdependent Progress of Hemolysis, Body Iron Accumulation, and Insufficient Erythropoietin Production in Rats

Cadmium Induces Anemia through Interdependent Progress of Hemolysis, Body Iron Accumulation, and Insufficient Erythropoietin Production in Rats

Kadmi̇yum Ve Etanolün Li̇pi̇d Peroksi̇dasyon, İz Element Düzeyleri̇ Ve Bi̇yoki̇myasal Göstergeler Üzeri̇ne Etki̇si̇ : Effects of Cadmium and Ethanol on Lipid Peroxidation, Trace Element Levels and Biochemical

Relationship between ceruloplasmin and Cu status involving metallothionein induced by several heavy metals in the mouse

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