API E

Alpha-tocopherol is the primary form of vitamin E that is preferentially used by the human body to meet appropriate dietary requirements.

In particular, the RRR-alpha-tocopherol (or sometimes called the d-alpha-tocopherol stereoisomer) stereoisomer is considered the natural formation of alpha-tocopherol and generally exhibits the greatest bioavailability out of all of the alpha-tocopherol stereoisomers.

Moreover, RRR-alpha-tocopherol acetate is a relatively stabilized form of vitamin E that is most commonly used as a food additive when needed 6.

Alpha-tocopherol acetate is subsequently most commonly indicated for dietary supplementation in individuals who may demonstrate a genuine deficiency in vitamin E. Vitamin E itself is naturally found in various foods, added to others, or used in commercially available products as a dietary supplement.

The recommended dietary allowances (RDAs) for vitamin E alpha-tocopherol are: males = 4 mg (6 IU) females = 4 mg (6 IU) in ages 0-6 months, males = 5 mg (7.5 IU) females = 5 mg (7.5 IU) in ages 7-12 months, males = 6 mg (9 IU) females = 6 mg (9 IU) in ages 1-3 years, males = 7 mg (10.4 IU) females = 7 mg (10.4 IU) in ages 4-8 years, males = 11 mg (16.4 IU) females = 11 mg (16.4 IU) in ages 9-13 years, males = 15 mg (22.4 IU) females = 15 mg (22.4 IU) pregnancy = 15 mg (22.4 IU) lactation = 19 mg (28.4 IU) in ages 14+ years 11.

Most individuals obtain adequate vitamin

E intake from their diets; genuine vitamin E deficiency is considered to be rare.

Nevertheless, vitamin E is known to be a fat-soluble antioxidant that has the capability to neutralize endogenous free radicals.

This biologic action of vitamin

E consequently continues to generate ongoing interest and study in whether or not its antioxidant abilities may be used to help assist in preventing or treating a number of different conditions like cardiovascular disease, ocular conditions, diabetes, cancer and more.

At the moment however, there exists a lack of formal data and evidence to support any such additional indications for vitamin E use.

In addition to any following information, owing to d-alpha-Tocopherol acetate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data.

E, known for its antioxidant activities, is protective against cardiovascular disease and some forms of cancer and has also demonstrated immune-enhancing effects.

It may be of limited benefit in some with asthma and rheumatoid arthritis.

It may be helpful in some neurological diseases including Alzheimer's, some eye disorders including cataracts, and diabetes and premenstrual syndrome.

It may also help protect skin from ultraviolet irradiation although claims that it reverses skin aging, enhances male fertility and exercise performance are poorly supported.

It may help relieve some muscle cramps.

In addition to any following information, owing to d-alpha-Tocopherol acetate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data.

E has antioxidant activity.

It may also have anti-atherogenic, antithrombotic, anticoagulant, neuroprotective, antiviral, immunomodulatory, cell membrane-stabilizing and antiproliferative actions.

E is a collective term used to describe eight separate forms, the best-known form being alpha-tocopherol.

E is a fat-soluble vitamin and is an important antioxidant.

It acts to protect cells against the effects of free radicals, which are potentially damaging by-products of the body's metabolism.

E is often used in skin creams and lotions because it is believed to play a role in encouraging skin healing and reducing scarring after injuries such as burns.

There are three specific situations when a vitamin E deficiency is likely to occur.

It is seen in persons who cannot absorb dietary fat, has been found in premature, very low birth weight infants (birth weights less than 1500 grams, or 3½ pounds), and is seen in individuals with rare disorders of fat metabolism.

A vitamin

E deficiency is usually characterized by neurological problems due to poor nerve conduction.

Symptoms may include infertility, neuromuscular impairment, menstrual problems, miscarriage and uterine degradation.

Preliminary research has led to a widely held belief that vitamin E may help prevent or delay coronary heart disease.

Antioxidants such as vitamin

E help protect against the damaging effects of free radicals, which may contribute to the development of chronic diseases such as cancer.

It also protects other fat-soluble vitamins (A and B group vitamins) from destruction by oxygen.

Low levels of vitamin

E have been linked to increased incidence of breast and colon cancer.

In addition to any following information, owing to d-alpha-Tocopherol acetate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data.

Although all forms of Vitamin

E exhibit antioxidant activity, it is known that the antioxidant activity of vitamin E is not sufficient to explain the vitamin's biological activity.

E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall.

It also appears to reduce oxLDL-induced apoptosis in human endothelial cells.

Oxidation of

LDL is a key early step in atherogenesis as it triggers a number of events which lead to the formation of atherosclerotic plaque.

In addition, vitamin E inhibits protein kinase C (PKC) activity.

PKC plays a role in smooth muscle cell proliferation, and, thus, the inhibition of PKC results in inhibition of smooth muscle cell proliferation, which is involved in atherogenesis.

E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 which lowers the adhesion of blood components to the endothelium.

In addition, vitamin E upregulates the expression of cytosolic phospholipase A2 and cyclooxygenase (COX)-1 which in turn enhances the release of prostacyclin.

Prostacyclin is a vasodilating factor and inhibitor of platelet aggregation and platelet release.

It is also known that platelet aggregation is mediated by a mechanism involving the binding of fibrinogen to the glycoprotein IIb/IIIa (GPIIb/IIIa) complex of platelets.

GPIIb/IIIa is the major membrane receptor protein that is key to the role of the platelet aggregation response.

GPIIb is the alpha-subunit of this platelet membrane protein.

Alpha-tocopherol downregulates

GPIIb promoter activity which results in reduction of GPIIb protein expression and decreased platelet aggregation.

E has also been found in culture to decrease plasma production of thrombin, a protein which binds to platelets and induces aggregation.

A metabolite of vitamin E called vitamin E quinone or alpha-tocopheryl quinone (TQ) is a potent anticoagulant.

This metabolite inhibits vitamin

K-dependent carboxylase, which is a major enzyme in the coagulation cascade.

The neuroprotective effects of vitamin

E are explained by its antioxidant effects.

Many disorders of the nervous system are caused by oxidative stress.

E protects against this stress, thereby protecting the nervouse system.

The immunomodulatory effects of Vitamin

E have been demonstrated in vitro, where alpha-tocopherol increases mitogenic response of T lymphocytes from aged mice.

The mechanism of this response by vitamin E is not well understood, however it has been suggested that vitamin E itself may have mitogenic activity independent of its antioxidant activity.

Lastly, the mechanism of action of vitamin E's antiviral effects (primarily against HIV-1) involves its antioxidant activity.

E reduces oxidative stress, which is thought to contribute to HIV-1 pathogenesis, as well as to the pathogenesis of other viral infections.

E also affects membrane integrity and fluidity and, since HIV-1 is a membraned virus, altering membrane fluidity of HIV-1 may interfere with its ability to bind to cell-receptor sites, thus decreasing its infectivity.

SEC14-like protein 3 Not Available Humans U SEC14-like protein 2 Not Available Humans U Nuclear receptor subfamily 1 group I member 2 Not Available Humans U Protein kinase C beta type Not Available Humans U Polyunsaturated fatty acid 5-lipoxygenase Not Available Humans U Protein kinase C alpha type Not Available Humans.

In addition to any following information, owing to d-alpha-Tocopherol acetate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data. 50-80% absorbed from gastrointestinal tract.

In addition to any following information, owing to d-alpha-Tocopherol acetate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data.

In addition to any following information, owing to d-alpha-Tocopherol acetate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data.

Hover over products below to view reaction partners D-alpha-Tocopherol acetate 13'-hydroxychromanol 13'-carboxychromanol CDMDHC CDMOHC CDMHHC CMBHC CEHC.

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Patients with hypercalcemia.

The recommended initial dose of calcium acetate for the adult dialysis patient is 2 capsules with each meal.

Increase the dose gradually to lower serum phosphorus levels to the target range, as long as hypercalcemia does not develop.

Most patients require 3-4 capsules with each meal.

Starting dose is 2 capsules with each meal.

Titrate the dose every 2-3 weeks until acceptable serum phosphorus level is reached.

Each capsule is of size ‘00el’ hard gelatin capsule shell with blue opaque cap and white opaque body imprinted with “667 mg” on cap and “IG 377” on body in black ink filled with white to off white powder.

Supplied in

Bottles of 60 (NDC 69097-862-03) and 200 (NDC 69097-862-83).

Store at 20° to 25°C (68° to 77°F) .

Calcium acetate capsules contain calcium acetate.

Animal reproduction studies have not been conducted with calcium acetate, and there are no adequate and well controlled studies of calcium acetate use in pregnant women.

Patients with end stage renal disease may develop hypercalcemia with calcium acetate treatment.

Maintenance of normal serum calcium levels is important for maternal and fetal well being.

Hypercalcemia during pregnancy may increase the risk for maternal and neonatal complications such as stillbirth, preterm delivery, and neonatal hypocalcemia and hypoparathyroidism.

Calcium acetate treatment, as recommended, is not expected to harm a fetus if maternal calcium levels are properly monitored during and following treatment.

A calcium acetate capsule contains calcium acetate and is excreted in human milk.

Human milk feeding by a mother receiving calcium acetate is not expected to harm an infant, provided maternal serum calcium levels are appropriately monitored.

Safety and effectiveness in pediatric patients have not been established.

Clinical studies of calcium acetate did not include sufficient numbers of subjects aged and over to determine whether they respond differently from younger subjects.

Other clinical experience has not identified differences in responses between elderly and younger patients.

In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.