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Vitamin E (Alpha-Tocopherol)

May 22, 2023Chemical pathologyLab Tests

Table of Contents

  • Vitamin E (alpha-Tocopherol)
      • Sample for Vitamin E (α-Tocopherol)
        • Precaution for Vitamin E
      • History of Vitamin E
      • Pathophysiology of Vitamin E
      • Sources of vitamin E are:
      • Metabolism of Vitamin E:
      • Due to Vitamin E deficiency:
      • Signs of Vitamin E toxicity:
        • Normal Vitamin E
      • Questions and answers:

Vitamin E (alpha-Tocopherol)

Sample for Vitamin E (α-Tocopherol)

  1. The patient’s plasma is needed. For plasma, take a sample in heparin.
  2. A fasting sample is preferred.
  3. The sample is stable at 4 °C for 4 weeks and at -20 or -70 °C for one year.
  4. Protect from light.

Precaution for Vitamin E

  1. Avoid the use of alcohol at least 24 hours before taking the blood sample.
  2. Protect the sample from light.

History of Vitamin E

  1. In 1920, the factor in vegetable oil was the reason for the deficient resorption in deficient rats.
  2. Later on, it was given the name of tocopherol.
  3. Vitamin E has several biologically active isomers.
  4. The word tocopherol is a Greek-derived name.
  5. Its fertility role is still questionable.
  6. α-tocopherol is the most common biologically active isomer in the blood.

Pathophysiology of Vitamin E

  1. This is a powerful antioxidant vitamin.
    1. Oxidants’ role is to cause disease, aging, and cleavage of fatty acids.
  2. This vitamin is soluble in fat solvents and insoluble in water.
  3. Its generic name is tocopherol which includes several biologically active isomers.
  4. α-tocopherol is the predominant isomer and is the biologically active form.
    1. It is viscous oil at room temperature.
    2. Stable to heat in the absence of oxygen.
  5. It plays a role in cellular respiration.
  6. Vitamin E contains 8 related natural compounds that are biosynthesized in plants, and these are abundant in vegetables.
    1. Eight Vitamin E subtypes are tocopherols and tocotrienols.
    2. Its most active unit is α-tocopherol.
  7. Its main function is antioxidants.

Isomers of Vitamin E:

  1. α-Tocopherol (Alpha-Tocopherol).
  2. β-Tocopherol (Beta-Tocopherol).
  3. γ-Tocopherol (Gamma-Tocopherol).
  4. δ-Tocopherol (Delta-Tocopherol).
  5. ζ-Tocopherol (Zeta-Tocopherol).
  6. ε-Tocopherol (Epsilon-Tocopherol).
  7. η-Tocopherol (Eta-Tocopherol).
  8. 8-Methyl-tocotrienol.

Absorption of vitamin E:

  1. Its absorption takes place in the presence of bile in the small intestine.
    1. Most of the tocopherol enters the bloodstream via lymph.
  2. So it is associated with chylomicron and very low-density lipoprotein.
  3. About 40% of the ingested tocopherol is absorbed.
  4. Physiologic requirements of vitamin E (Tocopherol) are increased with increasing polyunsaturated fatty acids in the diet.
  5. Absorbed vitamin E (tocopherol) is first associated with circulating chylomicron and VLDL.
  6. Some vitamin E (Tocopherol) is transferred to adipose tissue during triglyceride hydrolysis.

Sources of vitamin E are:

  1. Vegetable oils.
  2. Fresh leafy vegetables.
  3. Eggs and yolk.
  4. Legumes.
  5. Peanuts.
  6. Margarine.
  7. Most of it is stored in the adipose tissue.

Metabolism of Vitamin E:

  1. Vitamin E (Tocopherol) absorption, transportation, and storage are partially understood.
  2. Vitamin E (Tocopherol) is absorbed along with chylomicron and VLDL.
  3. Bile salt is needed for its absorption.
Vitamin E metabolism

Vitamin E metabolism

  1. When the normal dose of Vitamin E is given, a very small amount appears in the urine.
Vitamin E and Excretion

Vitamin E and Absorption

Functions of Vitamin E:

  1. Vitamin E (tocopherol) is an Antioxidant.
  2. The specific role of humans is unclear.
  3. It protects unsaturated fatty acids from peroxidation (it is the cleavage of fatty acids).
    1. Cleavage of fatty acids at their unsaturated sites by oxygen addition across the double bond and formation of free radicals.
  4. Protect from free radicals.
  5. Prevent the oxidation of vitamin A, DNA, and phospholipids of the cell membrane.
  6. Acts with selenium for the maintenance of cell membranes. This effect may be more neuronal.
  7. There is a role of vitamin E in protecting the RBCs membranes from oxidants stress.
  8. There is evidence to prevent retrolental fibroplasia,  intraventricular hemorrhage, and mortality of premature infants.
  9. Vitamin E may have a preventive role in cardiovascular disease.
  10. Vitamin E also plays a role in neurological diseases.

Due to Vitamin E deficiency:

  1. There is irritability and edema.
  2. There is peripheral neuropathy and ataxia.
  3. There is a degeneration of the spinal cord.
  4. Vitamin E protects the RBC’s cell membrane from oxidants.
    1. The anemia is due to the fragile RBC membrane, and there is no response to iron therapy.
  5. Mild Hemolytic anemia in infants.
  6. These symptoms due to its deficiency are rare except in the case of malabsorption.
  7. There is a loss of tendon reflexes.
  8. There may be pigmentary retinopathy.

Clinical presentation of vitamin E deficiency:

  1. The major symptom is mild hemolytic anemia.
  2. A relationship exists between vitamin E  deficiency and progressive loss of neurological function in infants and children with chronic cholestasis.
  3. Premature infants are supplemented with vitamin E to stabilize the RBCs membranes and prevent hemolytic anemia.
  4. It is found the relationship between vitamin E deficiency and progressive loss of neurological signs in infants and children with chronic cholestasis.
  5. The nervous system is very sensitive to vitamin E deficiency.
    1. Some signs of Vitamin E deficiency were axonal deterioration in the spinal cord, associated with gait disturbance and stability.
  6. Sterility is found in animal models.
  7. There is macrocytic megaloblastic anemia in α-Tocopherol deficiency.
  8. Diagnosis:
    1. α-Tocopherol concentration is <5 mg/L.

Signs of Vitamin E toxicity:

  1. There is decreased platelet aggregation.
  2. There may be impaired wound healing.
  3. There is impaired fibrinolysis.
  4. There may be hepatomegaly.
  5. There is creatinuria.
  6. Diagnosis:
    1. Infants receiving sufficient amounts of α-Tocopherol where serum level is >30 mg/L have an increased incidence of sepsis and necrotizing enterocolitis.
    2. The patients receiving a synthetic diet should be monitored to avoid Vitamin E toxicity.

Normal Vitamin E

Source 1

  1.  Some recommend > 0.5 mg / 100 ml.
  2. Premature neonates  = 0.31 to ± 0.06 mg/dL.
  3. 1 to 12 years = 0.3 to 0.9 mg/dL
  4. 13 to 19 years = 0.6 to 1.0 mg/dL
  5. Adult  = 0.5 to 1.8 mg/dL
  6. Deficiency =  <0.3 mg/dL
  7. Excess level  =  >4 mg/dL

Another source

  • Recommended daily for adults male = 10 mg/day.
    • For females = 8 mg/day.

Questions and answers:

Question 1: What is the main complication of vitamin E deficiency?
Show answer
Premature infants may develop hemolytic anemia.
Question 2: What is the main role of Vitamin E?
Show answer
Vitamin E is an antioxidant.

Possible References Used
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