Pantothenic acid is also known as vitamin B5. It is a component of coenzyme A (CoA), an essential coenzyme in a variety of reactions that sustain life. CoA is required for chemical reactions that generate energy from food (fat, carbohydrates, and proteins). The synthesis of essential fats, cholesterol, and steroid hormones requires CoA, as does the synthesis of the neurotransmitter, acetylcholine, and the hormone, melatonin. Heme, a component of hemoglobin, requires a CoA-containing compound for its synthesis. Metabolism of a number of drugs and toxins by the liver requires CoA.
Coenzyme A was named for its role in acetylation reactions. Most acetylated proteins in the body have been modified by the addition of an acetate group that was donated by CoA. Protein acetylation affects the 3-dimensional structure of proteins, potentially altering their function, the activity of peptide hormones, and appears to play a role in cell division and DNA replication. Protein acetylation also affects gene expression by facilitating the transcription of mRNA. A number of proteins are also modified by the attachment of long-chain fatty acids donated by CoA. These modifications are known as protein acylation, and appear to play a central role in cell signaling.
The acyl-carrier protein requires pantothenic acid in the form of phosphopantetheine for its activity as an enzyme. Both CoA and the acyl-carrier protein are required for the synthesis of fatty acids. Fatty acids are a component of some lipids, which are fat molecules essential for normal physiological function. Among these essential fats are sphingolipids, which are a component of the myelin sheath that enhances nerve transmission, and phospholipids in cell membranes.
Administration of pantothenic acid orally and application of pantothenol ointment to the skin have been shown to accelerate the closure of skin wounds and increase the strength of scar tissue in animals. Adding calcium-D-pantothenate to cultured human skin cells given an artificial wound increased the number of migrating skin cells and their speed of migration, effects likely to accelerate wound healing. However, little data exists in humans to support the findings of acceleratedwound healing in cell culture and animal studies. A randomized, double blind study examining the effect of supplementing patients undergoing surgery for tattoo removal with 1,000 mg of vitamin C and 200 mg of pantothenic acid could not document any significant improvement in thewound healing process in those that received the supplements.
A pantothenic acid derivative called pantethine has been reported by anumber of investigators to have a cholesterol lowering effect. Pantethine is actually two molecules of pantetheine joined by adisulfide bond (chemical bond between two molecules of sulfur). In the synthetic pathway of coenzyme A (CoA), pantethine is closer to CoA thanpantothenic acid, and is the functional component of CoA and acyl carrier proteins. Several studies found doses of 900 mg of pantethinedaily (300 mg, three times daily) to be significantly more effective than placebo in lowering total cholesterol and triglyceride levels in the blood of both diabetic and non-diabetic individuals. Pantethine was also found to lower cholesterol and triglyceride levels in diabetic patients on hemodialysis without adverse side effects. The low side effect profile of pantethine was especially attractive for hemodialysis patients because of the increased risk of drug toxicity in patients with renal (kidney) failure. Pantethine is not a vitamin; it is a derivative of pantothenic acid. The decision to use pantethine to treat elevated blood cholesterol or triglycerides should be made in collaboration with a qualified health care provider, who can provide appropriate follow up.
1. Weimann BI, Hermann D. Calcium D-Pantothenate. Int J Vitam Nutr Res. 1999 Mar;69(2):113-9.
The effect of calcium D-pantothenate on the migration, proliferation and protein synthesis of human dermal fibroblasts from three different donors was investigated. The migration of cells into a wounded area was dose-dependently stimulated by Ca D- pantothenate. The number of cells that migrated across the edge of the wound increased from 32 +/- 7 cells/mm without Ca D-pantothenate to 76 +/- 2 cells/mm with 100 mg/ml Ca D-pantothenate. Moreover, the mean migration distance per cell increased from 0.23 +/- 0.05 mm to 0.33 +/- 0.02 mm. The mean migration speed was calculated to be 10.5 mm/hour without and 15 mm/hour with Ca D-pantothenate. Cell proliferation was also dose-dependently stimulated. The final cell densities were 1.2 to 1.6-fold higher in cultures containing 100 mg/ml Ca D-pantothenate. The protein synthesis was modulated, since two unidentified proteins were more strongly expressed in pantothenate supplemented cultures. In conclusion, Ca D-pantothenate accelerates the wound healing process by increasing the number of migrating cells, their distance and hence their speed. In addition, cell division is increased and the protein synthesis changed. These results suggest that higher quantities of pantothenate are locally required to enhance wound healing.
2. Vaxman F, Olender S, Lambert A, Nisand G, Aprahamian M, Bruch JF. Effect of Pantothenic Acid and Ascorbic Acid Supplementation on Human Skin Wound Healing Process. Eur Surg Res. 1995;27(3):158-66.
This study aimed at testing human skin wound healing improvement by a 21-day supplementation of 1.0 g ascorbic acid (AA) and 0.2 g pantothenic acid (PA). 49 patients undergoing surgery for tattoos, by the successive resections procedure, entered a double-blind, prospective and randomized study. Tests performed on both skin and scars determined: hydroxyproline concentrations, number of fibroblasts, trace element contents and mechanical properties. In the 18 supplemented patients, it was shown that in skin (day 8) Fe increased (p < 0.05) and Mn decreased (p < 0.05); in scars (day 21), Cu (p = 0.07) and Mn (p < 0.01) decreased, and Mg (p < 0.05) increased; the mechanical properties of scars in group A were significantly correlated to their contents in Fe, Cu and Zn, whereas no correlation was shown in group B. In blood, AA increased after surgery with supplementation, whereas it decreased in controls. Although no major improvement of the would healing process could be documented in this study, our results suggest that the benefit of AA and PA supplementation could be due to the variations of the trace elements, as they are correlated to mechanical properties of the scars.
3. Atamna H, Killilea DW. Mineral and Vitamin Deficiencies Can Accelerate the Mitochondrial Decay of Aging. Mol Aspects Med. 2005 Aug-Oct;26(4-5):363-78.
Mitochondrial oxidative decay, which is a major contributor to aging, is accelerated by many common micronutrient deficiencies. One major mechanism is inhibition of the pathway of heme biosynthesis in mitochondria, which causes a deficit of heme-a. Heme-a, only found in Complex IV, is selectively diminished, resulting in oxidant leakage and accelerated mitochondrial decay, which leads to DNA damage, neural decay, and aging. We emphasize those deficiencies, which appear to cause damage through this mechanism, particularly minerals such as iron (25% of menstruating women ingest <50% of the RDA) or zinc (10% of the population ingest <50% of the RDA). Several vitamin deficiencies, such as biotin or pantothenic acid, also increase mitochondrial oxidants through this mechanism. Additionally, other minerals such as magnesium and manganese that play a role in mitochondrial metabolism, but do not affect heme directly, are discussed. An optimum intake of micronutrients could tune up metabolism and give a marked increase in health, particularly for the poor, elderly, and obese, at little cost.
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