Quosis

Uses

Arginine is an amino acid commonly found as a component of total parenteral nutrition.

Used for nutritional supplementation, also for treating dietary shortage or imbalance.

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

For the supplementation of total parenteral nutrition to prevent hyposelenemia .

HMG CoA reductase inhibitors mediated decreased level of Coenzyme Q10 in blood, Drug induced Myopathy, Protects body against free radical damage with its antioxidant property, Adjuvant therapy in cardiovascular disease especially in angina and congestive heart failure, Immune system depression, Cognitive decline, Useful in the management of Periodontal Disease

Quosis is also used to associated treatment for these conditions: Acromegaly, Gigantism, Hyperammonaemia, Hypophysectomy, Kidney Damage, Panhypopituitarism, Pituitary Dwarfism, Pituitary Neoplasms, Deficiencies in enzymes of the urea cycle, Pituitary trauma, Postsurgical craniopharyngioma, Problems of growth and stature, Nutritional supplementation, Amino acid supplementationNutritional supplementationMigraine

How Quosis works

Many of supplemental L-arginine's activities, including its possible anti-atherogenic actions, may be accounted for by its role as the precursor to nitric oxide or NO. NO is produced by all tissues of the body and plays very important roles in the cardiovascular system, immune system and nervous system. NO is formed from L-arginine via the enzyme nitric oxide synthase or synthetase (NOS), and the effects of NO are mainly mediated by 3,'5' -cyclic guanylate or cyclic GMP. NO activates the enzyme guanylate cyclase, which catalyzes the synthesis of cyclic GMP from guanosine triphosphate or GTP. Cyclic GMP is converted to guanylic acid via the enzyme cyclic GMP phosphodiesterase. NOS is a heme-containing enzyme with some sequences similar to cytochrome P-450 reductase. Several isoforms of NOS exist, two of which are constitutive and one of which is inducible by immunological stimuli. The constitutive NOS found in the vascular endothelium is designated eNOS and that present in the brain, spinal cord and peripheral nervous system is designated nNOS. The form of NOS induced by immunological or inflammatory stimuli is known as iNOS. iNOS may be expressed constitutively in select tissues such as lung epithelium. All the nitric oxide synthases use NADPH (reduced nicotinamide adenine dinucleotide phosphate) and oxygen (O2) as cosubstrates, as well as the cofactors FAD (flavin adenine dinucleotide), FMN (flavin mononucleotide), tetrahydrobiopterin and heme. Interestingly, ascorbic acid appears to enhance NOS activity by increasing intracellular tetrahydrobiopterin. eNOS and nNOS synthesize NO in response to an increased concentration of calcium ions or in some cases in response to calcium-independent stimuli, such as shear stress. In vitro studies of NOS indicate that the Km of the enzyme for L-arginine is in the micromolar range. The concentration of L-arginine in endothelial cells, as well as in other cells, and in plasma is in the millimolar range. What this means is that, under physiological conditions, NOS is saturated with its L-arginine substrate. In other words, L-arginine would not be expected to be rate-limiting for the enzyme, and it would not appear that supraphysiological levels of L-arginine which could occur with oral supplementation of the amino acid^would make any difference with regard to NO production. The reaction would appear to have reached its maximum level. However, in vivo studies have demonstrated that, under certain conditions, e.g. hypercholesterolemia, supplemental L-arginine could enhance endothelial-dependent vasodilation and NO production.

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 .

Ubidecarenone is an essential cofactor in the mitochondrial electron transport chain. Its functions are the acceptance of electrons from the complex I and II and this activity is vital for the production of ATP. It acts as a mobile redox agent shuttling electrons and protons in the electron transport chain. Ubidecarenone also presents antioxidant activity in mitochondria and cellular membranes, protecting against peroxidation of lipid membranes as well as inhibiting oxidation of LDL-cholesterol.

Dosage

Quosis dosage

The recommended dose of Co-enzyme Q10 is:

For Co-enzyme Q10 deficiency:150 mg daily.

For mitochondrial disorders:150-160 mg, or 2 mg/kg/day.

For heart failure in adults:100 mg per day divided into 2 or 3 doses.

For recent myocardial infarction:120 mg daily in 2 divided doses.

For high blood pressure:120-200 mg per day divided into 2 doses.

For isolated systolic hypertension:60 mg twice daily.

For preventing migraine headache:100 mg three times daily.

For Parkinsons disease:300 mg, 600 mg, 1200 mg and 2400 mg per day in 3-4 divided doses.

For infertility in men:200-300 mg per day.

For muscular dystrophy:100 mg per day.

Dividing the total daily dose by taking smaller amounts two or three times a day instead of a large amount all at once can help to reduce side effects.

Side Effects

Coenzyme Q10 is well tolerated and having no significant side effects. Mild gastrointestinal symptoms such as nausea, diarrhea and epigastric distress have been reported.

Toxicity

Oral supplementation with L-arginine at doses up to 15 grams daily are generally well tolerated. The most common adverse reactions of higher doses from 15 to 30 grams daily are nausea, abdominal cramps and diarrhea. Some may experience these symptoms at lower doses.

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.

There have not been reports of adverse events of diet supplementation with ubidecarenone. The normal side effects reported in humans are related to the gastrointestinal tract.

Precaution

Supplemental Coenzyme Q10 may improve beta-cell function and glycemic control in type II diabetics. Therefore, those diabetic patients who do use supplemental Coenzyme Q10 should determine by appropriate monitoring if they need to make any adjustments in their diabetic medications.

Interaction

Warfarin: Supplemental Coenzyme Q10 may decrease the effectiveness of Warfarin.

Statins: The statin drugs are known to decrease Coenzyme Q10 levels in humans.

Doxorubicin: Coenzyme Q10 may increase the cardiotoxicity of doxorubicin.

Antidiabetic medications: Coenzyme Q10 may improve glycemic control in some type II diabetics. If this were to occur, antidiabetic medications might need appropriate adjusting

Volume of Distribution

Ubidecarenone is distributed to the various tissues of the body and it is able to enter the brain. In preclinical studies with intravenous administration of ubidecarenone, it is reported a volume of distribution of 20.4 L/kg which reflects its ability to penetrate extensively into organs and tissues. AS a general rule, tissues with high-energy requirements or metabolic activity tend to presents higher amounts of ubidecarenone, these organs can be heart, kidney, liver and muscle.

Elimination Route

Absorbed from the lumen of the small intestine into the enterocytes. Absorption is efficient and occurs by an active transport mechanism.

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

Ubidecarenone is absorbed from the small intestine into the lymphatics and then it can enter the blood. The hydrophobicity and large molecular weight limit its absorption making it very poor and variable depending on the food intake and the number of lipids presented in the food. The absorption is lower in the presence of an empty stomach and greater in presence of high lipid food diet. The daily dosage of ubidecarenone presents the reach of maximal serum concentration by reaching a plateau after three weeks. The pharmacokinetic properties may vary between different brands but studies have reported an AUC of 11.51 mcg h/ml and a Cmax of 0.32 mcg/ml at a time of 7.9 h.

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.

The pharmacokinetic properties may vary between different brands but studies have reported a half-life of ubidecarenone of 21.7 h.

Clearance

In preclinical studies with intravenous administration of ubidecarenone, it is reported a total clearance of 1.18 ml h/kg which was indicative of a prolonged elimination.

Elimination Route

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 main elimination route of ubidecarenone is through the bile. After its oral administration, over 60% of the dose is excreted in the feces in the form of unchanged ubidecarenone and a small fraction of the metabolites. In the urine, ubidecarenone is bound to saposin B protein and represents only 8.3% of the total administered dose.

Pregnancy & Breastfeeding use

Because of lack of information on long-term safety, pregnant women and nursing mothers should avoid Coenzyme Q10.

Contraindication

Patients with a known hypersensitivity to any component of this product

Storage Condition

Store in a cool & dry place, protect from light & moisture. Keep out of the reach of children.

Innovators Monograph

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