Folic Acid 1.5 mg, Lycopene 6000 mcg, Selenium 60 mcg, Vitamin A 2500 IU, Vitamin B6 3 mg, Vitamin C 50 mg, Vitamin E 25 IU Hard-gelatin capsules

Folic acid acts on megaloblastic bone marrow to produce a normoblastic marrow.

In man, an exogenous source of folate is required for nucleoprotein synthesis and the maintenance of normal erythropoiesis. Folic acid is the precursor of tetrahydrofolic acid, which is involved as a cofactor for transformylation reactions in the biosynthesis of purines and thymidylates of nucleic acids. Impairment of thymidylate synthesis in patients with folic acid deficiency is thought to account for the defective deoxyribonucleic acid (DNA) synthesis that leads to megaloblast formation and megaloblastic and macrocytic anemias.

Absorption — Folic acid is absorbed from the small intestine, primarily from the proximal portion. Folic acid appears in the plasma approximately 15 to 30 minutes after an oral dose; peak levels are generally reached within 1 hour.

Distribution — Folic acid as well as its physiologically active metabolite, L-5-methyl tetrahydro folate (L-5-MTHF), can be bound to plasma proteins when entering the systemic circulation. The fraction of folic acid bound to plasma proteins, particularly albumin, ranges between ~50% to 64%. The volume of distribution of L-5-MTHF is estimated to be 32.0 L. Tetrahydrofolic acid derivatives are distributed to all body tissues but are stored primarily in the liver. Cerebrospinal fluid levels of folic acid are several times greater than serum levels of the drug.

Metabolism — The first step in the metabolism of folic acid is its reduction to dihydrofolate via dihydrofolate reductase. Subsequently, dihydrofolate is further reduced to tetrahydrofolate (THF). THF is further converted to methylene-THF by serine-hydroxymethyltransferase and reduced to physiologically active L-5-MTHF via methylenetetrahydrofolate reductase (MTHFR).

Elimination — After intravenous administration, folic acid is rapidly cleared from the plasma. Following oral administration, majority of the dose was recovered in the urine. A majority of the metabolic products appeared in the urine after 6 hours; excretion was generally complete within 24 hours. Small amounts of orally administered folic acid have also been recovered in the feces.

Pyridoxal phosphate and pyridoxamine phosphate are active vitamin B6 coenzymes involved in amino-acid metabolism. B6 also contributes to neurotransmitter synthesis, glycogen metabolism and hemoglobin formation.

Vitamin B6 is absorbed in the jejunum. Phosphorylated forms are dephosphorylated before free B6 enters by passive diffusion. The NIH review describes similar absorption from foods and supplements; much of a large pharmacological dose is rapidly eliminated in urine. This physiology does not supply a measured half-life for this formulation.

Selenium is incorporated into selenoproteins including glutathione peroxidases and thioredoxin reductases. These proteins contribute to thyroid-hormone metabolism and protection against oxidative damage.

Absorbed organic and inorganic selenium is metabolized toward an intermediate used to synthesize selenocysteine. A substantial body pool is in skeletal muscle. Urinary excretion is the main mechanism maintaining balance; excretion through feces and lungs also increases at high intake. This general physiology does not establish equal bioavailability among selenium compounds.

Ascorbic acid supports collagen, carnitine and neurotransmitter biosynthesis and acts as a physiological antioxidant. It also improves absorption of nonheme iron. These biological functions do not establish a disease-treatment benefit for an individual formulation.

Oral absorption is dose-dependent: the NIH review reports about 70–90% at intakes of 30–180 mg/day and less than 50% above 1 g/day. Plasma and tissue concentrations are tightly regulated, and absorbed unmetabolized ascorbic acid is eliminated in urine. Oral data cannot be used as intravenous vitamin C pharmacokinetics.

Vitamin E encompasses fat-soluble compounds with antioxidant activity. Alpha-tocopherol is the form recognized as meeting human requirements; biological activity differs among tocopherols and tocotrienols.

Vitamin E forms are absorbed in the small intestine and taken up by the liver. Hepatic alpha-tocopherol transfer protein preferentially returns alpha-tocopherol to the circulation, while the liver metabolizes and excretes other forms. This selective handling means different vitamin E forms should not be assigned identical pharmacokinetic values.

Vitamin A supports cell differentiation and normal epithelial tissues and is required for visual signaling through rhodopsin. Preformed retinoids and provitamin A carotenoids are different nutritional sources of vitamin A activity.

Vitamin A forms enter intestinal micelles and are absorbed by duodenal cells. Retinyl esters and provitamin A carotenoids undergo conversion to retinol at different stages of uptake. The NIH review reports variable absorption across forms; these nutrient findings should not be treated as equivalent bioavailability for retinol, beta-carotene and retinoid medicines.