Mechanisms and Regulation of Intestinal Uptake and Transfer of Iron

Pr, Flanagan

doi:10.1111/apa.1989.78.s361.21

Cited by 29 publications

(12 citation statements)

References 67 publications

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“…Subjects consuming a low iron diet had a tissue lead concentration significantly higher than subjects consuming adequate iron. Furthermore, excess iron uptake decreased blood, femur and kidney lead concentrations whereas low iron increased the tissue lead concentration [94][95][96][97][98] . Rapid improvement in the development scores of infants after iron therapy has been reported 99) .…”

Section: Ironmentioning

confidence: 99%

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Kalia¹,

Flora²

2005

Journal of Occupational Health

267

161

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Strategies for Safe and Effective Therapeutic Measures for Arsenic and LeadPoisoning: Kiran Kalia, et al. Department of Biosciences, Sardar Patel University, IndiaExposure to toxic metals remains a widespread occupational and environmental problem in world. There have been a number of reports in the recent past suggesting an incidence of childhood lead poisoning and chronic arsenic poisoning due to contaminated drinking water in many areas of West Bengal in India and Bangladesh has become a national calamity. Low level metal exposure in humans is caused by air, food and water intake. Lead and arsenic generally interferes with a number of body functions such as the central nervous system (CNS), the haematopoietic system, liver and kidneys. Over the past few decades there has been growing awareness and concern that the toxic biochemical and functional effects are occurring at a lower level of metal exposure than those that produce overt clinical and pathological signs and symptoms. Despite many years of research, we are still far from an effective treatment of chronic plumbism and arsenicosis. Medical treatment of acute and chronic lead and arsenic toxicity is furnished by chelating agents. Chelating agents are organic compounds capable of linking together metal ions to form complex ring-like structures called chelates. They have been used clinically as antidotes for acute and chronic poisoning. 2, 3-dimercaprol (BAL) has long been the mainstay of chelation therapy for lead or arsenic poisoning. Meso 2, 3, -dimercaptosuccinic acid (DMSA) has been tried successfully in animals as well as in a few cases of human lead and arsenic poisoning. DMSA could be a safe and effective method for treating lead or arsenic poisoning, but one of the major disadvantages of chelation with DMSA has been its Review inability to remove lead from the intracellular sites because of its lipophobic nature. Further, it does not provide protection in terms of clinical/ biochemical recovery. A new trend in chelation therapy is to use combined treatment. This includes the use of structurally different chelators or a combination of an adjuvant and a chelator to provide better clinical/ biochemical recovery in addition to lead mobilization. The present review article attempts to provide update information about the current strategies being adopted for a safe, effective and specific treatment for two major toxic metals or metalloid.

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Section: Ironmentioning

confidence: 99%

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Kalia¹,

Flora²

2005

Journal of Occupational Health

267

161

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“…Dietary iron absorption takes place in the first portion of the small intestine [1]. Iron in food can be found either as a constituent of heme or as inorganic iron.…”

Section: Background and Aimsmentioning

confidence: 99%

“…The first step in iron absorption, known as the uptake step [1], involves the passage of iron from the intestinal lumen into the enterocyte. Intestinal cells have a plasma membrane Fe 3+ reduction system that facilitates inorganic iron absorption: the extracellular reduction of Fe 3+ to Fe 2+ prior to uptake was demonstrated in mouse intestine [5,6] and cultured intestinal cells [7,8].…”

Section: Background and Aimsmentioning

confidence: 99%

Effect of Copper, Cadmium, Mercury, Manganese and Lead on Fe<sup>2+</sup> and Fe<sup>3+</sup> Absorption in Perfused Mouse Intestine

Iturri¹,

Núñez

1998

Digestion

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Body iron homeostasis is maintained by the regulation of iron absorption in the first portion of the small intestine. Previous studies have shown that some trace metal cations may have an inhibitory effect on inorganic iron absorption. In view of the possible nutritional and toxicological implications of this inhibition, we decided to study the effect of Cu²⁺, Cd²⁺, Hg²⁺, Pb²⁺, and Mn²⁺ on Fe²⁺ and Fe³⁺ intestinal uptake. To that end, the duodenal portion of the mouse intestine was perfused with 1 µM ⁵⁵Fe either in the 2+ or 3+ redox state, in the absence or presence of a 10-fold molar excess of Cd²⁺, Cu²⁺, Hg²⁺, Mn²⁺, or Pb²⁺. It was found that Cd²⁺ and Cu²⁺, but not Hg²⁺, Mn²⁺, or Pb²⁺, significantly inhibited the uptake of Fe²⁺ (p < 0.001). Surprisingly, the observed inhibition by Cu²⁺ and Cd²⁺ was dependent on the iron redox state, since neither cation inhibited Fe³⁺ uptake by mouse duodenum. Similarly, no inhibition of Fe³⁺ uptake was observed with a 10-fold molar excess of Hg²⁺, Mn²⁺, or Pb²⁺. These results indicate that inhibition of iron uptake by Cu²⁺ and Cd²⁺ takes place only in a reducing environment. Therefore, under the common oxidative conditions found in nutrients no inhibition of non-heme Fe uptake by Cu²⁺ and Cd²⁺, as well as Mn²⁺, Hg²⁺ and Pb²⁺ is to be expected. We propose either that Fe²⁺ and Fe³⁺ are transported through two different mechanisms, or that the enterocyte-mediated reduction of Fe³⁺, and the ensuing transport of Fe²⁺ are processes coupled in such a way that they are refractory to inhibition by Cu²⁺ and Cd²⁺.

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“…It has been known for many years that intestinal mucosal cells rapidly adjust to decreases in body iron stores to facilitate the absorption of a greater fraction of the dietary iron (Bannerman et al, 1962). Although extensively studied, the molecular events that lead to the increased iron absorption are still unclear (Flanagan, 1989).…”

Section: Introductionmentioning

confidence: 99%

Alterations in the mucosal processing of iron in response to very-short-term dietary iron depletion and repletion

Topham

Eads

Butler

1992

Biochemical Journal

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The transfer of control rats to a low-iron diet for only 24 h resulted in a 2-fold increase in iron uptake by brush-border membrane vesicles. Extension of the low-iron feeding period to 72 h or 2 weeks resulted in only small additional increases in iron uptake by vesicle preparations. In contrast, the transfer of iron-deficient rats to a control diet resulted in a progressive decrease in iron uptake by vesicles that reached a level equivalent to that of control rats in 2 weeks. 59Fe labelling of detergent extracts of these vesicle preparations provided evidence for the presence of an iron-binding protein composed of subunits of 52,000 Da. The changes in the 59Fe labelling of this protein component were consistent with the changes observed in iron uptake by intact brush-border membrane vesicles. The 59Fe-labelling profiles of mucosal ferritin and transferrin from a test dose also were changed substantially in response to very-short-term alterations in dietary iron. Even though changes in dietary iron rapidly altered iron uptake by brush-border membrane vesicles and the incorporation of 59Fe from the test dose into mucosal transferrin, changes in the incorporation of 59Fe into mucosal ferritin best reflected the actual changes in the transfer of iron from dose to plasma.

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Mechanisms and Regulation of Intestinal Uptake and Transfer of Iron

Cited by 29 publications

References 67 publications

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Effect of Copper, Cadmium, Mercury, Manganese and Lead on Fe<sup>2+</sup> and Fe<sup>3+</sup> Absorption in Perfused Mouse Intestine

Alterations in the mucosal processing of iron in response to very-short-term dietary iron depletion and repletion

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