Nervex Mechanism of Action

Vitamins.
Pharmacology: Pharmacodynamics: Thiamine (as the coenzyme, thiamine pyrophosphate) is associated with carbohydrate metabolism. Thiamine pyrophosphate also acts as a co-enzyme in the direct oxidative pathway of glucose metabolism. In thiamine deficiency, pyruvic and lactic acids accumulate in the tissues. The pyruvate ion is involved in the biosynthesis of acetylcholine via its conversion to acetyl co-enzyme A through a thiamine-dependent process. In thiamine deficiency, therefore, there are effects on the central nervous system due either to the effect on acetylcholine synthesis or to the lactate and pyruvate accumulation. Deficiency of thiamine results in fatigue, anorexia, gastro-intestinal disturbances, tachycardia, irritability and neurological symptoms. Gross deficiency of thiamine (and other Vitamin B group factors) leads to the condition beri-beri.
Vitamin B₆ (Pyridoxine): Pyridoxine, once absorbed, is rapidly converted to the co-enzymes pyridoxal phosphate and pyridoxamine phosphate which play an essential role in protein metabolism. Convulsions and hypochromic anaemia have occurred in infants deficient in pyridoxine.
Vitamin B₁₂ (Cyanocobalamin): Vitamin B₁₂ is present in the body mainly as methylcobalamin and as adenosylcobalamin and hydroxocobalamin. These act as co-enzymes in the trans methylation of homocysteine to methionine; in the isomerisation of methylmalonyl co-enzyme to succinyl co-enzyme and with folate in several metabolic pathways respectively. Deficiency of Vitamin B₁₂ interferes with haemopoiesis and produces megaloblastic anaemia.
Vitamin E: Vitamin E deficiency has been linked to disorders such as cystic fibrosis where fat absorption is impaired. It is essential for the normal function of the muscular system and the blood.
Folic Acid: Folic acid is reduced in the body to tetrahydrofolate which is a co-enzyme for various metabolic processes, including the synthesis of purine and pyrimidine nucleotides and hence in the synthesis of DNA. It is also involved in some amino acid conversion and in the formation and utilisation of formate. Deficiency of folic acid leads to megaloblastic anaemia.
Pharmacokinetics: Vitamin B₁ (Thiamine): Thiamine is absorbed from the gastro-intestinal tract and is widely distributed to most body tissues. Amounts in excess of the body's requirements are not stored but excreted in the urine as unchanged thiamine or its metabolites.
Vitamin B₆ (Pyridoxine): Pyridoxine is absorbed from the gastro-intestinal tract and converted to the active pyridoxal phosphate which is bound to plasma proteins. It is excreted in the urine as 4-pyridoxic acid.
Vitamin B₁₂ (Cyanocobalamin): Cyanocobalamin is absorbed from the gastro-intestinal tract and is extensively bound to specific plasma proteins. A study with labelled Vitamin B₁₂, showed it was quickly taken up by the intestinal mucosa and held there for 2-3 hours. Peak concentrations in the blood and tissues did not occur until 8-12 hours after dosage with maximum concentrations in the liver within 24 hours. Cobalamins are stored in the liver, excreted in the bile and undergo enterohepatic recycling. Part of a dose is excreted in the urine, most of it in the first eight hours.
Vitamin E: Vitamin E is absorbed from the gastro-intestinal tract. Most appears in the lymph and is then widely distributed to all tissues. Most of a dose is slowly excreted in the bile and the remainder is eliminated in the urine as glucuronides of tocopheronic acid or other metabolites.
Folic Acid: Folic acid is absorbed mainly from the proximal part of the small intestine. Folate polyglutamates are considered to be deconjugated to monoglutamates during absorption. Folic acid rapidly appears in the blood where it is extensively bound to plasma proteins. Some folic acid is distributed in body tissues, some is excreted as folate in the urine and some is stored in the liver as folate.