Important minerals that are asked in biochemistry exams

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Important Minerals in Biochemistry Exams

Sources: Lippincott Illustrated Reviews: Biochemistry 8th ed, Ganong's Review of Medical Physiology 26th ed, Goldman-Cecil Medicine

Overview

Minerals are divided into macrominerals (needed in larger amounts: Ca, P, Mg, Na, K, Cl) and microminerals/trace elements (needed in minute amounts). The 15 trace minerals essential to health are: iron, zinc, copper, chromium, selenium, iodine, fluorine, manganese, molybdenum, cobalt, nickel, tin, silicon, vanadium, and arsenic - but only the first 10 have compelling evidence in humans.

1. Iron (Fe)

Body content: 3-4 g total; ~70% in hemoglobin.

Functions:

Component of hemoglobin, myoglobin, cytochromes
Part of Fe-S proteins of the electron transport chain
Cofactor for hydroxylases (e.g., prolyl hydroxylase in collagen synthesis)
Note: Free ionic Fe is toxic - generates hydroxyl radicals (ROS)

Absorption & Transport:

Heme iron (animal): absorbed via heme carrier protein (HCP) → heme oxygenase releases Fe²⁺
Non-heme iron (plants, Fe³⁺): reduced to Fe²⁺ by duodenal cytochrome b (Dcytb, requires Vitamin C as coenzyme) → absorbed via DMT-1 (divalent metal transporter-1)
Storage: Fe³⁺ stored by ferritin (up to 4,500 Fe³⁺/molecule); overflow stored as insoluble hemosiderin
Export: ferroportin (only known Fe exporter) → oxidized by hephaestin (Cu-containing) → binds transferrin (2 Fe³⁺/molecule, normally 1/3 saturated)
Recycling: Macrophages recycle Fe from old RBCs via ferroportin + ceruloplasmin (Cu-containing plasma ferroxidase) → meets ~90% of daily need
Regulation: Hepatic hepcidin is the master regulator - induces degradation of ferroportin, reducing Fe export. Suppressed when Fe is deficient.

Key protein	Role
DMT-1	Apical uptake of nonheme Fe²⁺
Ferritin	Intracellular Fe³⁺ storage
Ferroportin	Only cellular Fe exporter
Hephaestin	Oxidizes Fe²⁺ → Fe³⁺ at enterocyte basolateral membrane
Transferrin (Tf)	Plasma Fe³⁺ transport (2 Fe³⁺/molecule)
Ceruloplasmin	Oxidizes Fe²⁺ → Fe³⁺ in plasma (macrophages)
Hepcidin	Master regulator; degrades ferroportin

Deficiency: Microcytic, hypochromic anemia - most common anemia; serum ferritin low, Tf saturation low, TIBC elevated

Excess / Toxicity:

Hereditary hemochromatosis (HH): AR disorder (HFE gene mutation) → "bronze diabetes" (hyperpigmentation + hyperglycemia), liver damage, heart disease; tx: phlebotomy / chelation
Acute poisoning: most common cause of poisoning death in children <6 years; tx: chelation

2. Zinc (Zn)

Functions:

Zinc fingers - supersecondary structures in transcription factors that bind DNA and regulate gene expression
Cofactor for hundreds of enzymes:
- Alcohol dehydrogenase (ethanol → acetaldehyde)
- Carbonic anhydrase (bicarbonate buffer system)
- ALA dehydratase (heme synthesis - inhibited by lead, which displaces Zn)
- Superoxide dismutase (Cu/Zn-SOD, cytosolic form)
Needed in metabolism of Vitamin A (night vision)

Dietary sources: Meat, fish, eggs, dairy. Phytates (in grains, seeds, legumes) irreversibly bind Zn and impair absorption.

Deficiency:

Skin ulcers, depressed immune responses, hypogonadal dwarfism
Poor wound healing, growth retardation, alopecia, ageusia (loss of taste), anosmia
Acrodermatitis enteropathica - AR disorder; defect in intestinal Zn transporter. Triad: periacral/periorificial dermatitis, alopecia, diarrhea

3. Copper (Cu)

Functions:

Cofactor for cuproenzymes:
- Ceruloplasmin (plasma ferroxidase)
- Hephaestin (intestinal ferroxidase)
- Cytochrome c oxidase (Complex IV of ETC)
- Cu/Zn-SOD (superoxide dismutase)
- Lysyl oxidase (cross-linking of collagen and elastin)
- Dopamine β-hydroxylase (catecholamine synthesis)
- Tyrosinase (melanin synthesis)

Deficiency: Anemia (because Cu needed for Fe mobilization via ceruloplasmin/hephaestin), changes in ossification, neurological problems

Genetic disorders:

Disease	Gene	Defect	Features
Menkes disease	ATP7A (X-linked recessive)	Defect in Cu absorption/transport; systemic Cu deficiency	Kinky/steely hair, neurodegeneration, seizures, connective tissue defects; low serum Cu and ceruloplasmin
Wilson disease	ATP7B (AR)	Defect in Cu incorporation into ceruloplasmin + biliary excretion; Cu accumulates in tissues	Liver damage, Kayser-Fleischer rings in cornea, neuropsychiatric symptoms; low ceruloplasmin, high urinary Cu

4. Iodine (I)

Functions: Essential component of thyroid hormones (T3 and T4). Incorporated via thyroid peroxidase (TPO).

Dietary sources: Dairy, seafood, meat; iodized salt has greatly reduced deficiency worldwide.

Deficiency:

Goiter (thyroid enlargement from excessive TSH stimulation)
Hypothyroidism: fatigue, weight gain, decreased thermogenesis and metabolic rate
Congenital hypothyroidism (fetal/infant): cretinism - irreversible intellectual disability, hearing loss, spasticity, short stature

Excess: Graves disease (most common hyperthyroidism) - TSH-receptor antibody → nervousness, weight loss, tachycardia, exophthalmos, goiter. Over-ingestion of iodine supplements can also cause hyperthyroidism (UL = 1.1 g/day adults).

5. Selenium (Se)

Functions: Present in ~25 human selenoproteins as selenocysteine (derived from serine):

Glutathione peroxidase - reduces H₂O₂ to H₂O (antioxidant defense)
Thioredoxin reductase - reduces thioredoxin (coenzyme of ribonucleotide reductase)
Deiodinases - remove iodine from thyroid hormones (activation/deactivation of T3/T4)

Dietary sources: Meat, dairy, grains (content depends on soil Se content)

Deficiency: Keshan disease - endemic dilated cardiomyopathy in Se-deficient areas of China

Toxicity (selenosis): Brittle nails, brittle hair, cutaneous and neurological effects (UL = 400 μg/day adults)

6. Chromium (Cr)

Functions: Potentiates the action of insulin (mechanism not fully understood). Assists glucose metabolism.

Sources: Fruits, vegetables, dairy, meat

Deficiency: Insulin resistance (impaired glucose tolerance)

7. Fluorine (F)

Functions:

As fluoride (F⁻): replaces the hydroxyl group (-OH) in hydroxyapatite → forms fluoroapatite, which is more resistant to acid dissolution by oral bacteria
Reduces incidence of dental caries

Deficiency: Increased incidence of dental caries

8. Manganese (Mn)

Functions: Cofactor for several enzymes including:

Pyruvate carboxylase (OAA synthesis)
Mn-SOD (mitochondrial superoxide dismutase)
Arginase (urea cycle)

Sources: Whole grains, legumes, nuts, tea

Deficiency: Rare in humans. Toxicity from excess Mn can cause neurological symptoms resembling Parkinsonism.

9. Molybdenum (Mo)

Functions: Cofactor for a small number of oxidases (e.g., xanthine oxidase, sulfite oxidase)

Sources: Legumes

Note: No known dietary deficiency syndrome. Low toxicity (UL = 2 mg/day).

10. Cobalt (Co)

Functions: Essential solely as a component of Vitamin B₁₂ (cobalamin). An isolated cobalt deficiency syndrome has not been described; deficiency manifests as B₁₂ deficiency → megaloblastic anemia.

Calcium (Ca) - Macromineral

Absorption: 30-80% of ingested Ca absorbed; regulated by 1,25-dihydroxycholecalciferol (calcitriol) - increases in Ca deficiency, decreases in excess

Functions: Bone/teeth structure, muscle contraction, nerve conduction, blood clotting, second messenger (calmodulin), enzyme cofactor

Regulation: PTH, calcitonin, Vitamin D

Quick Exam Summary Table

Mineral	Key Role	Deficiency	Excess/Disease	High-Yield Fact
Fe	Hb, ETC, hydroxylases	Microcytic hypochromic anemia	Hemochromatosis (bronze diabetes)	Hepcidin controls ferroportin
Zn	Zn fingers, 100s enzymes	Dwarfism, immune deficiency, acrodermatitis enteropathica	Rare	ALA dehydratase inhibited by Pb displacing Zn
Cu	Ceruloplasmin, lysyl oxidase, ETC	Anemia, bone changes	Menkes (AR XL, low Cu), Wilson (AR, Cu overload)	Cu needed for Fe export from cells
I	Thyroid hormones	Goiter, cretinism	Graves disease	TPO uses I; iodized salt prevents deficiency
Se	Glutathione peroxidase, deiodinases	Keshan disease (cardiomyopathy)	Selenosis (brittle nails/hair)	Selenocysteine = 21st amino acid
Cr	Potentiates insulin	Insulin resistance	-	Mechanism unknown
F	Fluoroapatite in enamel	Dental caries	Dental/skeletal fluorosis	Replaces -OH in hydroxyapatite
Mn	Pyruvate carboxylase, Mn-SOD	Rare	Parkinsonism-like	Mitochondrial SOD uses Mn
Mo	Xanthine oxidase	None described	Low toxicity	Legumes are main dietary source
Co	Vitamin B₁₂ only	Megaloblastic anemia	Cardiomyopathy (beer drinkers)	No isolated Co deficiency - always B₁₂

High-yield exam points:

Hepcidin is the master Fe regulator - suppressed in Fe deficiency, induced by Fe overload/inflammation
Vitamin C enhances non-heme Fe absorption (Dcytb coenzyme: Fe³⁺ → Fe²⁺)
Phytates reduce Zn (and Fe) absorption from plant foods
Lead poisoning inhibits ALA dehydratase by displacing Zn (plus inhibits ferrochelatase) → sideroblastic-type anemia
Menkes vs Wilson: both Cu disorders; Menkes = low Cu (can't absorb/transport it); Wilson = high tissue Cu (can't excrete it)
Selenium's key enzyme is glutathione peroxidase - antioxidant defense
Acrodermatitis enteropathica = Zn deficiency (AR transporter defect): dermatitis + alopecia + diarrhea triad
Keshan disease = Se deficiency → dilated cardiomyopathy

Sources: Lippincott Illustrated Reviews: Biochemistry 8th ed, pp. 1114-1127; Ganong's Review of Medical Physiology 26th ed; Goldman-Cecil Medicine 26th ed

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