Copper 500 mcg, Folic Acid 100 mcg, Iodine 100 mcg, Lycopene 2000 mcg, Niacinamide 25 mg, Selenium 35 mcg, Vitamin B12 1 mcg, Vitamin B6 1.5 mg Syrup

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.

Vitamin B12 supplies cofactors for methionine synthase and methylmalonyl-CoA mutase. These reactions support methionine formation and conversion of methylmalonyl-CoA to succinyl-CoA. B12 is involved in DNA synthesis, red-cell formation and nervous-system function.

Free B12 combines with intrinsic factor and is taken up in the distal ileum. Absorption becomes less efficient as the dose exceeds intrinsic-factor capacity; the NIH review reports about 2% absorption at 500 micrograms and 1.3% at 1,000 micrograms. Cyanocobalamin and hydroxocobalamin are converted into active cobalamin forms. These are oral nutrient data, not injectable-product pharmacokinetics.

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.

Niacin supplies precursors for NAD and NADP. These coenzymes participate in cellular oxidation-reduction reactions, energy metabolism and biosynthetic processes. This nutrient role should not be confused with evidence for a lipid-lowering effect of every niacin form.

Ingested niacin is absorbed mainly in the small intestine, with some stomach absorption. Tissues convert physiological amounts to NAD. Excess is metabolized in the liver to methylated and oxidized products that are eliminated in urine; very high intake can also produce urinary excretion of unchanged nicotinic acid or nicotinamide.

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.

Copper is a cofactor in enzymes involved in energy production, iron metabolism, connective-tissue synthesis and neurotransmitter processing. Copper-containing superoxide dismutases participate in defense against oxidative damage.

Dietary copper is absorbed primarily in the upper small intestine. Ceruloplasmin carries most plasma copper. Intestinal uptake and liver secretion into bile regulate copper balance; bile is the major elimination route and urinary loss is smaller. This general nutrient disposition does not establish salt-specific bioavailability.

Iodine is a constituent of the thyroid hormones T4 and T3. These hormones regulate metabolic activity and are important for normal skeletal and nervous-system development.

Iodide is rapidly and almost completely absorbed from the stomach and duodenum. Ingested iodate is reduced to iodide before absorption. The thyroid concentrates circulating iodide for hormone synthesis, and most of the remainder is eliminated in urine. This oral nutrient reference does not characterize topical povidone-iodine or radiopharmaceuticals.