Trace elements

Overview

Trace elements are minerals that are required in small amounts to maintain normal physiological processes and function. They include iron, copper, zinc, iodine, selenium, and sulfur. Deficiency or excess of these elements can result in disease states due to alterations in physiological and biochemical processes.

Trace element Main function Deficiency Excess
Iron
Copper
Zinc
Iodine
Selenium
  • Cofactor for
    • Glutathione peroxidase
    • Iodothyronine deiodinase 2
  • Nausea, vomiting, diarrhea
  • Nail changes
  • Peripheral neuropathy
  • Fatigue
Sulfur

Iron

General

  • RDA: 10 mg/d (only 10% of iron is absorbed from the intestines)
  • Iron stores in the body
    • Total body iron content is ∼ 3 g in and ∼ 6 g in .
    • Total iron exists in two forms:
  • Dietary iron
    • Heme iron: from meat
    • Non-heme iron: from plants
  • Free iron can lead to reactive oxygen species via the Fenton reaction.
    • H2O2 + Fe2+ → OH- + Fe3+ + OH(hydroxyl radical)
    • Hydroxyl radicals → oxidative stressDNA damage

Iron absorption and transport

  • Iron absorption
    • Occurs in the duodenum and upper jejunum
    • The enzyme hepcidin regulates intestinal absorption of iron.
      • Hepcidin is synthesized in the liver
      • Increased body stores of ironhepcidinprevention of iron absorption
      • Iron deficiencyhepcidiniron absorption
    • Ferric iron (non-heme iron, Fe3+) is mainly reduced to ferrous iron (Fe2+) and then absorbed.
      • Vitamin C increases absorption (converts Fe3+ → Fe2+).
      • Calcium decreases absorption (due to chelation of iron).
      • A minority of iron is absorbed as ferric iron (Fe3+).
    • Heme iron can be directly absorbed into intestinal cells.
  • Iron transport

Iron storage, recycling, and loss

References:[1][2][3]

Function

Deficiency

For more details regarding the clinical features, diagnosis, and etiology of iron deficiency, see the learning card on iron deficiency anemia.

Excess

Copper

General

  • RDA: 900 μg/d
  • Source: meat, fish, poultry, vegetables, grains, legumes (e.g., lentils, beans)
  • Metabolism
    • Absorbed in the stomach and small intestine
      • Absorbed by active transport and passive diffusion
      • Exported from enterocytes via Menkes P-type ATPase
      • Binds albumin and is transported as part of the enterohepatic circulation
      • Transported by ceruloplasmin from the liver to peripheral tissue
    • Stored primarily in the liver and brain. Small amounts are stored in the heart, kidney, and pancreas.

Function

Deficiency

Excess

Zinc

General

  • RDA: 8–11 mg/d
  • Source: poultry, oysters, fish, meat, zinc-fortified food products (e.g., cereals), nuts
  • Metabolism

Function

  • Protein structure
    • Forms bonds between cysteine and histidine
    • Forms zinc finger transcription factors
  • Aids in maintenance and stability of the nuclear membrane
  • Essential part of many enzymes (> 70), including alkaline phosphatase, carbonic anhydrase, metallothionein, superoxide dismutase, ACE, and collagenases

Deficiency

Excess

  • Causes
    • Rare, but can develop due to excess zinc intake
  • Clinical features

References:[4]

Iodine

General

  • RDA: 150 μg/d
  • Source: seafood, seaweed, plants grown in iodine-rich soil, water, vegetables, iodized table salt
  • Metabolism
  • Elemental iodine can be used as a disinfectant.

Function

Iodine deficiency

Iodine excess

Selenium

General

  • RDA: 55 μg/d
  • Source: meat, seafood, grains and seeds (e.g., brazil nut)
  • Metabolism
    • Present in two forms (in animals): seleno-methionine and seleno-cysteine
    • Absorbed in the small intestine
    • Stored as seleno-methionine
    • Active form: seleno-cysteine
    • Excreted in the urine

Function

  • Cofactor for enzymes such as glutathione peroxidase , and iodothyronine deiodinase 2 (thyroid hormone production)

Selenium plays an important role in neutralizing oxidant stress as part of the glutathione peroxidase.

Deficiency

Excess

  • Causes: excess selenium intake (→ selenosis)
  • Clinical features
    • Nausea, vomiting, diarrhea
    • Hair loss
    • Nail changes
    • Fatigue
    • Peripheral neuropathy

Sulfur

General

  • Source: meat, eggs, nuts, salmon, leafy green vegetables (e.g., kale, spinach), legumes

Function

  • Form disulfide bonds (between cysteine residues)
    • Integral part in the tertiary structure of proteins
  • Present in methionine, cysteine, homocysteine, cystine, and taurine
  • Present in thiamine and biotin
  • Present in coenzyme-A
  • Present in keratin (aids in maintenance of skin, hair, and nails)
  • Essential for collagen synthesis

Deficiency

  • Causes
    • Deficiency is very rare.
    • Diet based on products grown in sulfur-depleted soils
    • Low-protein diets
  • Clinical features

Excess

  • Causes: Excess consumption of sulfur-rich foods
  • Clinical features
  • 1. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Philadelphia, PA: Elsevier Saunders; 2014.
  • 2. Soe-Lin S, Apte SS, Andriopoulos B Jr. Nramp1 promotes efficient macrophage recycling of iron following erythrophagocytosis in vivo. Proc Natl Acad Sci U S A. 2009; 106(14): pp. 5960–5965. doi: 10.1073/pnas.0900808106.
  • 3. University of Washington. Iron Absorption. https://courses.washington.edu/conj/bess/iron/iron.htm. Updated February 28, 2017. Accessed February 28, 2017.
  • 4. Dela Rosa KM. Acrodermatitis Enteropathica. In: James WD. Acrodermatitis Enteropathica. New York, NY: WebMD. https://emedicine.medscape.com/article/1102575. Updated November 12, 2018. Accessed December 29, 2018.
  • 5. Leung AM, Braverman LE. Consequences of excess iodine. Nat Rev Endocrinol. 2013; 10(3): pp. 136–142. doi: 10.1038/nrendo.2013.251.
  • 6. Markou K, Georgopoulos N, Kyriazopoulou V, Vagenakis AG. Iodine-Induced Hypothyroidism. Thyroid. 2001; 11(5): pp. 501–510. doi: 10.1089/105072501300176462.
last updated 05/23/2019
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