Minerals Flashcards
Sources and function of chromium
Sources: liver, processed meats, whole grain cereals, brewer’s yeast and nuts
Function:
The exact function of chromium within the human body is unknown.
It has been proposed that trivalent chromium (Cr3+) functions as a cofactor for an oligopeptide called chromomodulin.
Biologically active chromomodulin is reported to enhance the effects of insulin on target tissues.
Chromium deficiency and toxicity
Deficiency: Potential chromium deficiencies have been reported and symptoms resemble those of diabetes mellitus with impaired glucose tolerance and increased requirements for insulin.
Toxicity:
There are no known toxicities associated with the dietary intake of trivalent chromium.
In contrast, hexavalent chromium (Cr6+) is a known carcinogen.
Hexavalent chromium exposure is most likely to occur in an industrial setting as chromium has been used in the paint and die industry.
Sources and function of Copper
Sources: organ meats, shellfish, whole-grain cereals, fruits, and certain vegetables.
Functions:
There are a number of proteins and enzymes that have copper as a cofactor.
The most important of these are cytochrome C oxidase, superoxide dismutase (copper/zinc form), lysyl oxidase, ceruloplasmin (ferrioxidase), and tyrosinase.
Copper deficiencies
Dietary - one of the most common signs of copper deficiency is anemia linked to the role of copper-containing ferrioxidases like ceruloplasmin in iron mobilization.Such anemias are unresponsive to iron, but respond to copper.
Individuals at risk for copper deficiency include infants fed cow’s milk (low in copper), individuals with malabsorption symptoms, or iatrogenically through strict, but incomplete dietary therapies.
Inherited - Menkes disease is caused by a deficiency of a copper-transporting ATPase found in many cells throughout the body, including enterocytes where copper becomes trapped and fails to enter the circulation.
The clinical features of Menkes disease include intractable seizures connective tissue disorders, subdural hemorrhage and hair abnormalities (“kinky hair”).
Copper toxicities
Symptoms typically involve abdominal pain, nausea, vomiting, and diarrhea.
Individuals with Wilson’s disease caused by a defect in copper excretion from the body in the bile are at risk for copper toxicity.
Copper accumulation in the liver of patients with Wilson’s disease can lead to liver failure.
Copper accumulation in the brain of Wilson’s syndrome patients can also lead to neuropsychiatric symptoms.
Fluorine sources and function
Sources: seafood, tea, fluorinated water
Function: Fluoride does not function as a enzyme cofactor, but instead is incorporated into mineralized tissues of bones and teeth displacing OH groups of hydroxyapatite in forming fluoroapatite hardening tooth enamel and stabilizing mineralized bone.
Fluorine deficiency and toxicity
Deficiency: Inadequate fluoride intake leads to an increased risk of dental caries. In contrast, there is little evidence to suggest that fluorination of water has a beneficial effect on bone mineralization.
Toxicity:
Fluoride is toxic in high doses.
Fluorosis in children (abdominal pain, nausea) can be caused by swallowing excessive amounts of toothpaste while brushing.
Fluorosis can also be characterized by mottling and pitting of permanent teeth in adults.
Iodine sources and function
Sources: seafood, iodized salt, eggs, cheese
Function:
Iodine is an important substituent of the thyroid hormones thyroxine (t4) and triiodothyronine (T3).
Iodine is taken up from the blood into the thyroid gland where it is incorporated into thyroglobulin.
Breakdown of thyroglobulin by lysosomal enzymes produced the thyroid hormones that are stored and released as needed.
Thyroid hormones regulate growth, development, metabolism, and reproductive function.
Iodine deficiency and toxicity
Deficiency:
Symptoms of iodine deficiency include mental retardation, hypothyroidism, and goiter.
Iodine deficiency is considered the most common cause of preventable brain damage worldwide
Toxicity:
Acute iodine toxicity is associated with ingestion of large amounts of iodine can cause burning of mouth, throat, and stomach and subsequent, nausea, vomiting and diarrhea.
Acute toxicity can also result in cyanosis and coma.
Excess iodine intake can also lead to hyperthyroidism characterized by weight loss, tachycardia, muscle weakness and warm skin.
Iron sources and function
Sources: meats, fish, enriched grains and cereals (though plant sources can have problems with bioavailability)
Function: Iron is a critical component of heme-containing proteins and iron-sulfur proteins.
Iron deficiency and toxicity
Deficiency:
Iron deficiency tends to be more prevalent in children, pre-menopausal women (due to iron loss during menstruation) and in pregnant woman (due to diversion to the fetus).
Other symptoms of iron deficiency include pica, glossitis, angular cheilosis
Toxicity: Excess iron leads to hemochromatosis which can be characterized by liver cirrhosis, diabetes mellitus, cardiomyopathy, bronze skin pigmentation, and hypogonadism.
Iron overload can have genetic underpinnings as in hemochromatosis, or be iatrogenic where it can be caused by chronic transfusions.
Accidental overdose associated with ingestion of iron-containing products (supplements) is a frequent cause of poisoning in children under 6 years of age.
Initial symptoms of acute toxicity include abdominal pain, nausea, vomiting, and tarry stools but may progress to CNS damage, cirrhosis and other organ damage with time.
Manganese sources and function
Sources: whole grain cereals, pineapple, nuts, tea, tomatoes
Function:
Manganese is a component of a relatively small number of enzymes: glycosyl-transferases, phosphoenolpyruvate carboxykinase, and manganese superoxide dismutase.
Manganese deficiency and toxicity
Deficiency: Naturally occurring manganese deficiency has not been reported in humans, though deficiencies in animals can result in growth retardation, congenital bone malformations, and defects in carbohydrate and fat metabolism.
Toxicity:
Manganese toxicities have been reported in welders and smelters who inhale manganese dust.
Symptoms are similar to Parkinson’s disease including tremors and difficulty walking.
Psychiatric symptoms have also been observed with manganese toxicity.
Molybdenum sources and functions
Sources: milk, legumes, whole grain bread and cereals, dark green vegetables.
Functions: Molybdenum is a component of xanthine oxidase, sulfite oxidase and aldehyde oxidase.
Molybdenum toxicities and deficiencies
Deficiencies:
Dietary molybdenum deficiency has never been reported in healthy individuals.
Acquired molybdenum deficiency has been reported for a patient with Crohn’s disease on total parenteral nutrition without adequate molybdenum. Symptoms included tachycardia, tachypnea, headache, nausea, vomiting, and coma.
Inherited deficiencies in the formation of the molybdenum cofactor (Moco) used by the enzymes above have been reported with the major impact on the activity of sulfite oxidase, which plays a role in the metabolism of cysteine and methionine. Defects in the formation of Moco cause severe neurological dysfunction characterized by cerebral atrophy, mental retardation, and intractable seizures.
Toxicities: Few
