Pantothenic acid is present in all living cells with particularly high concentrations in the liver, kidney, adrenal gland, brain and heart.
Approximately 85% of pantothenic acid in food is present as coenzyme A. During digestion, coenzyme A is hydrolyzed in a series of enzymatic reactions to produce pantothenic acid which is then absorbed by passive diffusion or (at low levels) via a sodium dependent active uptake process.
As a water-soluble vitamin, up to 50% of pantothenic acid in food is lost during processing and cooking. It is relatively stable during storage.
The average dietary intake of pantothenic acid in the United States is 5 to 10 mg/day.
The principal supplemental form of pantothenic acid is synthetic calcium or sodium-D-pantothenate.
Panthenol (also called dexpanthenol and panthoderm) is the stable alcoholic form of pantothenic acid and is commonly available in haircare and skincare products. Panthenol is well absorbed through the skin and is rapidly enzymatically oxidized to pantothenic acid in the body.
Pantethine is a pantothenic acid derivative and is available in the United States as a supplement. Pantethine is sold as a drug in Europe and Japan used to lower cholesterol and triglyceride concentrations. Please see the Pantethine Vitamin & Herb University summary for more information.
Pantothenic acid (vitamin B5) is an essential component of coenzyme A (CoA) and acyl carrier protein (ACP). In both CoA and ACP, a derivative of pantothenic acid, 4'-phosphopantetheine, forms the active portion of the compound. COA is required for the chemical reactions that produce energy from carbohydrates, fats, and proteins and for the synthesis of essential fats, cholesterol, certain hormones, and the neurotransmitter acetylcholine. ACP is involved in the synthesis of fatty acids.
The principal functions of pantothenic acid are through CoA which is required for synthesis of essential fats, sterols, steroid hormones, melatonin, acetylcholine, and heme (a part of hemoglobin and many metabolic proteins).
CoA participates in acetylation of proteins, which has been found to influence the localization, stability, and activity of proteins.
ACP requires pantothenic acid (in the form of 4'-phosphopantetheine) for fatty acid synthesis. CoA is also involved in fatty acid synthesis.
Pantothenic acid and its derivatives reduce oxidative stress by promoting synthesis and preventing degradation of glutathione, an antioxidant peptide.
Functions for topical use of panthenol may include activation of fibroblast proliferation (relevant to wound healing), acceleration of re-epithelization in wound healing, and anti-inflammatory effects.
Deficiency of pantothenic acid in humans is very rare and has been observed only in cases of severe malnutrition. Symptoms of deficiency include "burning-feet syndrome" characterized by burning or tingling sensations in the feet and lower legs.
Pantothenic acid deficiency in humans has been induced experimentally. Participants complained of headache, fatigue, insomnia, intestinal disturbances and numbness and tingling of hands and feet.
In experiments with mice, skin irritation and graying of fur was noted with pantothenic acid deficiency. Pantothenic acid supplements reversed these effects. Based on these experiments, panthenol has been added to some haircare products, although panthenol has not been found to restore hair color in humans.
Pantothenic acid is widely distributed in plant and animal food sources, mainly as coenzyme A. Rich sources include: organ meats (liver, kidney), yeast, egg yolk, cashew nuts, peanuts, whole grains, lentils, soybeans, brown rice, broccoli, and milk.
3 There are no known or reported interactions between oral pantothenic acid and drugs.
According to one monograph on Dexpanthenol given by parenteral (IM or IV) administration:
Panthenol should not be given with or within 12 hours of administration of parasympathomimetic drugs such as neostigmine (Prostigmin).
Some reports suggest that pantothenic acid may potentiate the miotic (construction of the pupil) effects of echothiophate iodide and isoflurophate anticholinesterase ophthalmic preparations. It is advisable to avoid the concomitant administration of these drugs and pantothenic acid.
In rare cases, the concomitant use of panthenol and opiates (narcotics), barbiturates (depressants/sedatives), or antibiotics may trigger allergic reactions of unknown cause.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Dexpanthenol pastille and benzydamine hydrochloride spray for the prevention of post-operative sore throat.
The efficacy of panthenol pastilles to reduce the incidence of post-anesthesia sore throat was investigated in 180 surgical patients, aged 15 to 70 years. The subjects were randomly assigned to receive 200 mg panthenol, a benzydamine hydrochloride throat spray, or four puffs of distilled water (placebo) 30 minutes prior to anesthesia. Symptoms were monitored for 24 hours after surgery. The group receiving the panthenol pastilles had a significant reduction of the incidence and severity of sore throat compared to the benzydamine hydrochloride and placebo group. Thus, panthenol pastilles containing 200 mg of panthenol provided significant protection against post-anesthesia sore throat. 4
Panthenol has been used topically to treat various dermatologic disorders. for decades principally in Europe. Panthenol is included in a variety of skincare products in the United States due to its beneficial effects. A review by Ebner and colleagues summarized the experimental evidence for beneficial effects of topical panthenol with skin abrasions, petty injuries, chronic ulcers, decubital ulcers, anal fissures, skin transplantation, scar treatment, non-severe burns, diaper dermatitis, and epithelial lesions. In a study of wound healing with 15 participants, 5% dexpanthenol (water in oil emulsion) significantly reduced erythema in wounds treated daily for 5 days. Tissue regeneration was more elastic and solid with dexpanthenol treatment. In two additional studies, 3 and 5% dexpanthenol formulations produced statistically significant epidermal regeneration acceleration compared to untreated (p<0.0004) and placebo (p<0.05) controls. The dexpanthenol preparation promoted regeneration of the epidermal barrier. Panthenol has also been shown to improve symptoms of irritated skin. Three studies investigating the efficacy of panthenol containing lotions demonstrated that 5% panthenol creams improved skin moisture and decreased irritation. More than 90% of participants positively rated the panthenol creams in these studies. 5
Pantothenic acid and pantothenol increase biosynthesis of glutathione by boosting cell energetics.
An in vitro study with human lymphoblastoic (Jurkat) cells investigated the mechanism of synthesis of glutathione by pantothenic acid. A protective effect of pantothenic acid and its derivatives was previously found during times of oxidative stress. Incubation of the cells with pantothenic acid or panthenol resulted in a significant increase in free glutathione concentrations, with little or no change in protein bound glutathione. Inhibitors of glutathione synthesis prevented this response, indicating that pantothenic acid stimulates the synthesis of new glutathione. 6
Protection by pantothenic acid aginst apoptosis and cell damage by oxygen free radicals - the role of glutathione.
Beneficial effects of pantothenic acid and panthenol have been reported under conditions when damage by reactive oxygen species might be suspected. Pantothenic acid and panthenol were found to exert a metabolic effect rather than acting as free radical scavengers. CoA and glutathione concentrations were substantially increased by pantothenic acid supplementation. Pantothenic acid also protected against degradation and oxidation of glutathione during irradiation of cells with UV light, which subjects the cells to increased concentrations of reactive oxygen species. UV irradiation induces apoptosis in human leukemic lymphocytes. Pre-incubation of human leukemic lymphocyte cells with pantothenic acid prevented apoptosis in a dose-dependent manner and increased the concentration of glutathione by more that 50%. Supplementation with panthenol protected against peroxidative changes in rats exposed to UV irradiation before death. These experiments suggest that pantothenic acid and its derivatives may exert protective effects during oxidative stress by promoting glutathione synthesis or preventing its degradation. 7
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