Mixaria

Mixaria Uses, Dosage, Side Effects, Food Interaction and all others data.

Copper is a transition metal and a trace element in the body. It is important to the function of many enzymes including cytochrome c oxidase, monoamine oxidase and superoxide dismutase . Copper is commonly used in contraceptive intrauterine devices (IUD) .

Copper is incorporated into many enzymes throughout the body as an essential part of their function . Copper ions are known to reduce fertility when released from copper-containing IUDs .

Iodine is commonly used as an antiseptic for minor cuts and abrasions, preventing infections that may result from contaminated wounds. Additionally, iodine has been studied in the treatment of fibrocystic disease and breast cancer.

Selenium is a trace metal in the human body particularly important as a component of glutathione peroxidase, an important enzyme in the prevention of cellular damage by free radicals and reactive oxygen species

Selenium is incorporated into many different selenoproteins which serve various functions throughout the body .

Vitamin D ultimately comprises a group of lipid-soluble secosteroids responsible for a variety of biological effects, some of which include increasing the intestinal absorption of calcium, magnesium, and phosphate. With reference to human use, there are 2 main forms of vitamin D - vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol). When non-specific references are made about 'vitamin d', the references are usually about the use of vitamin D3 and/or D2.

Vitamin D3 and D2 require hydroxylation in order to become biologically active in the human body. Since vitamin D can be endogenously synthesized in adequate amounts by most mammals exposed to sufficient quantities of sunlight, vitamin D functions like a hormone on vitamin D receptors to regulate calcium in opposition to parathyroid hormone. Vitamin D plays an essential physiological role in maintaining calcium homeostasis and metabolism. There are several different vitamin D supplements that are given to treat or to prevent osteomalacia and rickets, or to meet the daily criteria of vitamin D consumption.

The in vivo synthesis of the predominant two biologically active metabolites of vitamin D occurs in two steps. The first hydroxylation of vitamin D3 or D2 occurs in the liver to yield 25-hydroxyvitamin D while the second hydroxylation happens in the kidneys to give 1, 25-dihydroxyvitamin D . These vitamin D metabolites subsequently facilitate the active absorption of calcium and phosphorus in the small intestine, serving to increase serum calcium and phosphate levels sufficiently to allow bone mineralization . Conversely, these vitamin D metabolites also assist in mobilizing calcium and phosphate from bone and likely increase the reabsorption of calcium and perhaps also of phosphate via the renal tubules . There exists a period of 10 to 24 hours between the administration of vitamin D and the initiation of its action in the body due to the necessity of synthesis of the active vitamin D metabolites in the liver and kidneys . It is parathyroid hormone that is responsible for the regulation of such metabolism at the level of the kidneys .

Vitamin E Capsule is a Vitamin E preparation. Vitamin E acts as an antioxidant in the body. Vitamin E protects polyunsaturated fatty acids (which are components of cellular membrane) and other oxygen-sensitive substances such as vitamin A & vitamin C from oxidation. Vitamin E reacts with free radicals, which is the cause of oxidative damage to cell membranes, without the formation of another free radical in the process. The main pharmacological action of vitamin E in humans is its antioxidant effect.

In premature neonates irritability, edema, thrombosis and hemolytic anemia may be caused due to vitamin E deficiency. Creatinuria, ceroid deposition, muscle weakness, decreased erythrocyte survival or increased in vitro hemolysis by oxidizing agents have been identified in adults and children with low serum tocopherol concentrations.

Vitamin E is a collective term used to describe 8 separate fat soluble antioxidants, most commonly alpha-tocopherol. Vitamin E acts to protect cells against the effects of free radicals, which are potentially damaging by-products of the body's metabolism. Vitamin E deficiency is seen in persons with abetalipoproteinemia, premature, very low birth weight infants (birth weights less than 1500 grams, or 3½ pounds), cystic fibrosis, and cholestasis and severe liver disease. Preliminary research suggests vitamin E may help prevent or delay coronary heart disease and 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.

Trade Name Mixaria
Generic Di dalam + Vitamin E + Vitamin D + Vitamin C + Vitamin B + Vitamin B + Vitamin B + asam folat + zat besi + zink + copper + selenium + iodine + Vitamin K
Type Powder
Therapeutic Class
Manufacturer Meprofarm
Available Country Indonesia
Last Updated: September 19, 2023 at 7:00 am
Mixaria
Mixaria

Uses

Copper is a transition metal found in a variety of supplements and vitamins, including intravenous solutions for total parenteral nutrition (TPN).

For use in the supplementation of total parenteral nutrition and in contraception with intrauterine devices .

Iodine is an ingredient of nutritional supplements that is also used for disinfection.

Investigated for use/treatment in breast disorders (unspecified) and pain (acute or chronic).

Selenium is an ingredient found in a variety of supplements and vitamins.

For the supplementation of total parenteral nutrition to prevent hyposelenemia .

Vitamin D is an ingredient found in a variety of supplements and vitamins.

Vitamin D is indicated for use in the treatment of hypoparathyroidism, refractory rickets (also known as vitamin D resistant rickets), and familial hypophosphatemia .

As a dietary supplement:

  • Vitamin E deficiency resulting from impaired absorption.
  • Increased requirements due to diet rich in polyunsaturated fats.
  • For healthy hair & skin
  • As an Antioxidant
  • Hemolytic anemia due to Vitamin E deficiency

Therapeutic use

: Heavy metal poisoning, Hepatotoxin poisoning, Hemolytic anemia, Oxygen therapy and replacement therapy in nutritional deficiency states for the betterment of skin and hair.

Mixaria is also used to associated treatment for these conditions: Emergency Contraception, IUD, Trace Element Deficiency, Dietary supplementationInfection in minor cuts, scrapes, or burns, Antisepsis, Antimycotic, Prophylaxis of bacterial skin infectionsNutritional supplementationDeficiency, Vitamin DVitamin Deficiency, Long-chain omega-3 fatty acid supplementation, Dietary supplementation

How Mixaria works

Copper is absorbed from the gut via high affinity copper uptake protein and likely through low affinity copper uptake protein and natural resistance-associated macrophage protein-2 . It is believed that copper is reduced to the Cu1+ form prior to transport. Once inside the enterocyte, it is bound to copper transport protein ATOX1 which shuttles the ion to copper transporting ATPase-1 on the golgi membrane which take up copper into the golgi apparatus. Once copper has been secreted by enterocytes into the systemic circulation it remain largely bound by ceruloplasmin (65-90%), albumin (18%), and alpha 2-macroglobulin (12%).

Copper is an essential element in the body and is incorporated into many oxidase enzymes as a cofactor . It is also a component of zinc/copper super oxide dismutase, giving it an anti-oxidant role. Copper defiency occurs in Occipital Horn Syndrome and Menke's disease both of which are associated with impaired development of connective tissue due to the lack of copper to act as a cofactor in protein-lysine-6-oxidase. Menke's disease is also associated with progressive neurological impairment leading to death in infancy. The precise mechanisms of the effects of copper deficiency are vague due to the wide range of enzymes which use the ion as a cofactor.

Copper appears to reduce the viabilty and motility of spermatozoa . This reduces the likelihood of fertilization with a copper IUD, producing copper's contraceptive effect . The exact mechanism of copper's effect on sperm are unknown.

Molecular iodine is known to inhibit the induction and promotion of N-methyl-n-nitrosourea-induced mammary carcinogenesis, to regress 7,12-dimethylbenz(a)anthracene-induced breast tumors in rats.It has also been shown to have beneficial effects in fibrocystic human breast disease.

Selenium is first metabolized to selenophosphate and selenocysteine. Selenium incorporation is genetically encoded through the RNA sequence UGA . This sequence is recognized by RNA ste loop structures called selenocysteine inserting sequences (SECIS). These structures require the binding of SECIS binding proteins (SBP-2) to recognize selenocystiene. The specialized tRNA is first bound to a serine residue which is then enzymatically processed to a selylcysteyl-tRNA by selenocystiene sythase using selenophosphate as a selenium donor. Other unidentified proteins are required as part of the binding of this tRNA to the ribosome. Selenoproteins appear to be necessary for life as mice with the specialized tRNA gene knocked out exhibited early embryonic lethality .

The most important selenoproteins seem to be the glutathione peroxidases and thioredoxin reductases which are part of the body's defenses againts reactive oxygen species (ROS) . The importance of selenium in these anti-oxidant proteins has been implicated in the reduction of atherosclerosis by preventing the oxidation of low density lipoprotein . Selenium supplementation is also being investigated in the prevention of cancer and has been suggested to be beneficial to immune function .

Most individuals naturally generate adequate amounts of vitamin D through ordinary dietary intake of vitamin D (in some foods like eggs, fish, and cheese) and natural photochemical conversion of the vitamin D3 precursor 7-dehydrocholesterol in the skin via exposure to sunlight.

Conversely, vitamin D deficiency can often occur from a combination of insufficient exposure to sunlight, inadequate dietary intake of vitamin D, genetic defects with endogenous vitamin D receptor, or even severe liver or kidney disease . Such deficiency is known for resulting in conditions like rickets or osteomalacia, all of which reflect inadequate mineralization of bone, enhanced compensatory skeletal demineralization, resultant decreased calcium ion blood concentrations, and increases in the production and secretion of parathyroid hormone . Increases in parathyroid hormone stimulates the mobilization of skeletal calcium and the renal excretion of phosphorus . This enhanced mobilization of skeletal calcium leads towards porotic bone conditions .

Ordinarily, while vitamin D3 is made naturally via photochemical processes in the skin, both itself and vitamin D2 can be found in various food and pharmaceutical sources as dietary supplements. The principal biological function of vitamin D is the maintenance of normal levels of serum calcium and phosphorus in the bloodstream by enhancing the efficacy of the small intestine to absorb these minerals from the diet . At the liver, vitamin D3 or D2 is hydroxylated to 25-hydroxyvitamin D and then finally to the primary active metabolite 1,25-dihydroxyvitamin D in the kidney via further hydroxylation . This final metabolite binds to endogenous vitamin d receptors, which results in a variety of regulatory roles - including maintaining calcium balance, the regulation of parathyroid hormone, the promotion of the renal reabsorption of calcium, increased intestinal absorption of calcium and phosphorus, and increased calcium and phosphorus mobilization of calcium and phosphorus from bone to plasma to maintain balanced levels of each in bone and the plasma .

The mechanism of action for most of vitamin E's effects are still unknown. Vitamin E is an antioxidant, preventing free radical reactions with cell membranes. Though in some cases vitamin E has been shown to have pro-oxidant activity.

One mechanism of vitamin E's antioxidant effect is in the termination of lipid peroxidation. Vitamin E reacts with unstable lipid radicals, producing stable lipids and a relatively stable vitamin E radical. The vitamin E radical is then reduced back to stable vitamin E by reaction with ascorbate or glutathione.

Dosage

Mixaria dosage

Betterment of Cardiovascular health: 400 mg - 800 mg / day

Deficiency syndrome in adults: 200 mg - 400 mg / day

Deficiency syndrome in children: 200 mg / day

Thalassemia: 800 mg / day

Sickle-cell anemia: 400 mg / day

Betterment of Skin & Hair: 200 mg - 400 mg / day (Topical use is also established for beautification)

Chronic cold in adults: 200 mg / day

Side Effects

Overdoses (>1g) have been associated with minor side effects, including hypertension, fatigue, diarrhea and myopathy

Toxicity

Copper toxicity is belevied to be due to fenton-type redox reactions occuring with high copper concentrations which produce damaging reactive oxygen species .

Oral LD50 of 6700mg/kg in rats . Selenium exposure is teratogenic and can result in fetal death as tested in mice. Chronic toxicity is characterized by hair loss, white horizontal streaking on fingernails, paronchyia, fatigue, irritability, hyperreflexia, nausea, vomiting, garlic odor on breath, and metallic taste . Serum selenium correlates weakly with symtoms. Blood chemistry as well as liver and kidney function are normally unnaffected. Acute toxicity presents as stupor, respiratory depression, and hypotension. ST elevations and t-wave changes characteristic of myocardial infarction may be observed.

The use of pharmacological or nutraceutical vitamin d and/or even excessive dietary intake of vitamin d is contraindicated in patients with hypercalcemia, malabsorption syndrome, abnormal sensitivity to the toxic effects of vitamin d, and hypervitaminosis D .

Hypersensitivity to vitamin d is one plausible etiologic factor in infants with idiopathic hypercalcemia - a case in which vitamin d use must be strictly restricted .

As vitamin d intake is available via fortified foods, dietary supplements, and clinical drug sources, serum concentrations and therapeutic dosages should be reviewed regularly and readjusted as soon as there is clinical improvement . Dosage levels are required to be individualized on an individual patient by patient basis as caution must be exercised to prevent the presence of too much vitamin d in the body and the various potentially serious toxic effects associated with such circumstances .

In particular, the range between therapeutic and toxic doses is quite narrow in vitamin d resistant rickets . When high therapeutic doses are used, progress should be followed with frequent blood calcium determinations .

When treating hypoparathyroidism, intravenous calcium, parathyroid hormone, and/or dihydrotachysterol may be required .

Maintenance of normal serum phosphorus levels by dietary phosphate restriction and/or administration of aluminum gels as intestinal phosphate binders in those patients with hyperphosphatemia as frequently seen in renal osteodystrophy is essential to prevent metastatic calcification .

Mineral oil interferes with the absorption of lipid-soluble vitamins, including vitamin d preparations .

The administration of thiazide diuretics to hypoparathyroid patients who are concurrently being treated with vitamin d can result in hypercalcemia .

At this time, no long term animal studies have been performed to evaluate vitamin potential for carcinogens, mutagenesis, or fertility .

As various animal reproduction studies have demonstrated fetal abnormalities in several species associated with hypervitaminosis D, the use of vitamin d in excess of the recommended dietary allowance during normal pregnancy should be avoided . The safety in excess of 400 USP units of vitamin d daily during pregnancy has not been established . The abnormalities observed are similar to the supravalvular aortic stenosis syndrome described in infants that is characterized by supravalvular aortic stenosis, elfin facies, and mental retardation .

In a nursing mother given large doses of vitamin D, 25-hydroxycholecalciferol appeared in the milk and caused hypercalcemia in her child. Caution is subsequently required when contemplating the use of vitamin d in a nursing woman, and the necessity of monitoring infants' serum calcium concentration if vitamin d is administered to a breastfeeding woman .

Adverse reactions associated with the use of vitamin d are primarily linked to having hypervitaminosis D occurring [FDA Lanel]. In particular, hypervitaminosis D is characterized by effects specific effects on specific organ systems. At the renal system, hypervitaminosis D can cause impairment of renal function with polyuria, nocturne, polydipsia, hypercalciuria, reversible asotemia, hypertension, nephrocalcinosis, generalized vascular calcification, or even irreversible renal insufficiency which may result in death . Elsewhere, hypervitaminosis D can also cause CNS mental retardation . At the level of soft tissues, it can widespread calcification of the soft tissues, including the heart, blood vessels, renal tubules, and lungs . In the skeletal system, bone demineralization (osteoporosis) in adults can occur while a decline in the average rate of linear growth and increased mineralization of bones, dwarfism, vague aches, stiffness, and weakness can occur in infants and children . Finally, hypervitaminosis D can also lead to nausea, anorexia, and constipation at the gastrointestinal level as well as mild acidosis, anemia, or weight loss via metabolic processes .

The LD(50) in animals is unknown .

There is no data available for effects in pregnancy, breast feeding, hepatic impairment, or renal impairment. However, it appears that the process of vitamin E elimination is strict and self regulating enough that vitamin E toxicity is exceedingly rare. Studies showing adverse effects from excess vitamin E generally involve people consuming more than 1000mg/day for weeks to months.

Precaution

Vitamin E may enhance the anticoagulant activity of anticoagulant drugs. Caution is advised in premature infants with high dose Vitamin E supplementation, because of reported risk of necrotizing enterocilitis.

Interaction

Vitamin E may impair the absorption of Vitamin A. Vitamin K functions impairement happens at the level of prothrombin formation and potentiates the effect of Warfarin.

Volume of Distribution

0.41L/kg in premature neonates given a 20mg/kg intramuscular injection.

Elimination Route

Copper absorption varies inversely with intake. Absorption range is 12-65%.

Oral bioavailability of 90% when given as L-selenomethionine . Tmax of 9.17h.

Vitamin D3 and D2 are readily absorbed from the small intestine (proximal or distal) .

10-33% of deuterium labelled vitamin E is absorbed in the small intestine. Absorption of Vitamin E is dependant upon absorption of the fat in which it is dissolved. For patients with poor fat absorption, a water soluble form of vitamin E may need to be substituted such as tocopheryl polyethylene glycol-1000 succinate.

In other studies the oral bioavailability of alpha-tocopherol was 36%, gamma-tocotrienol was 9%. The time to maximum concentration was 9.7 hours for alpha-tocopherol and 2.4 hours for gamma-tocotrienol.

Half Life

Half life was observed to increase with chronic dosing time . For day 1-2 half life was 1.7 days. For day 2-3 half life was 3 days. For day 3-14 half life was 11.1 days.

Although certain studies suggest the half-life of 1,25-hydroxyvitamin D3 may be approximately 15 hours, the half-life of 25-hydroxyvitamin D3 appears to have a half-life of about 15 days . Intriguingly however, the half-lives of any particular administration of vitamin d can vary and in general the half-lives of vitamin D2 metabolites have been demonstrated to be shorter overall than vitamin D3 half-lives with this being affected by vitamin d binding protein concentrations and genotype in particular individuals .

44 hours in premature neonates given a 20mg/kg intramuscular injection. 12 minutes in intravenous injection of intestinal lymph.

Clearance

Some studies propose an estimated clearance rate for 1,25-dihydroxyvitamin D as 31 +/- 4 ml/min in healthy adults .

6.5mL/hr/kg in premature neonates given a 20mg/kg intramuscular injection.

Elimination Route

Copper appears to be eliminated primarily through bile .

Mainly excreted in urine as 1beta-methylseleno-N-acetyl-d-galactosamine and trimethylselenonium . The amount excreted as 1beta-methylseleno-N-acetyl-d-galactosamine plateaus at doses around 2microg after which the amount excreted as trimethylselenonium increases. Some selenium is also excreted in feces when given orally .

The primary excretion route of vitamin D is via the bile into the feces .

Alpha tocopherol is excreted in urine as well as bile in the feces mainly as a carboxyethyl-hydrochroman (CEHC) metabolite, but it can be excreted in it's natural form .

Pregnancy & Breastfeeding use

Use in pregnancy: Vitamin E may be used in pregnancy in the normally recommended dose but the safety of high dose therapy has not been established.

Use in lactation: There appears to be no contraindication to breast feeding by mothers taking the normally recommended dose.

Contraindication

No known contraindications found.

Special Warning

Use in Children: Vitamin E is safe for children

Acute Overdose

Large doses of vitamin E (more than 1 gm/day) have been reported to increase bleeding tendency in vitamin K deficient patients such as those taking oral anticoagulants.

Storage Condition

Store at a cool and dry place, Protect from light and moisture.

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