ZENTOKID​ ​ORAL LIQUID

Indications

• Vitamin B6 deficiency
• Isoniazid-induced neuropathy (prophylaxis and treatment)
• Idiopathic sideroblastic anaemia
• Prevention of penicillamine-induced neuropathy in Wilson's disease
• Metabolic diseases such as cystathioninuria and homocystinuria
• Premenstrual syndrome

Mechanism of action

Pyridoxine hydrochloride is converted in the body to pyridoxal phosphate, which is the active form of vitamin B6. It serves as a cofactor for more than 100 enzymatic reactions, particularly those involved in the metabolism of amino acids, the synthesis of neurotransmitters (such as serotonin, dopamine, and gamma-aminobutyric acid), and the production of hemoglobin. Its role in neurotransmitter synthesis makes it crucial for normal brain function and mood regulation.

Pharmacodynamics

Pyridoxine hydrochloride exerts its effects by facilitating the conversion of amino acids into neurotransmitters and is involved in the synthesis of heme. It impacts the metabolism of tryptophan to serotonin and is essential for the production of norepinephrine and gamma-aminobutyric acid, which are vital for proper neurological function. Deficiency of vitamin B6 can lead to neurological symptoms, including peripheral neuropathy and cognitive disturbances.

Pharmacokinetics

Pyridoxine hydrochloride is readily absorbed from the gastrointestinal tract. It is primarily metabolized in the liver, where it is converted to its active form, pyridoxal phosphate. The elimination half-life of pyridoxine is approximately 15-20 days, and it is excreted primarily through the urine. Renal impairment may affect the metabolism and excretion of pyridoxine, necessitating dose adjustments.

Contra-indications

• Hyperkalaemia
• Severe liver damage

Adverse effects

• Peripheral neuritis
• Hepatitis
• Hypoglycaemia
• Urine discolouration

Interactions

• Potassium aminobenzoate
• Isoniazid

Precautions

• Caution in renal impairment (increased risk of hyperkalaemia)
• Interrupt treatment during periods of low food intake (such as fasting, anorexia, and nausea) to reduce risk of hypoglycaemia
• Monitor liver function tests monthly during high-dose therapy

Pregnancy

Manufacturer advises avoiding use in pregnancy due to potential risk of birth defects; however, no adverse effects have been reported at normal dietary levels.

Breast-feeding

Theoretical risk of toxicity in infants if mothers take large doses.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Pyridoxine hydrochloride 10 mg tablets
• Pyridoxine hydrochloride 20 mg tablets
• Pyridoxine hydrochloride 50 mg tablets
• Pyridoxine hydrochloride oral solution 20 mg per 1 ml

Indications

• Vitamin B1 deficiency
• Wernicke-Korsakoff syndrome
• Beriberi
• Isoniazid-induced neuropathy (prophylaxis and treatment)
• Severe depletion or malabsorption of vitamins B and C

Dosage

Adults: For vitamin deficiency: 25–100 mg daily. For severe deficiency: 200–300 mg daily in divided doses. For

Mechanism of action

Thiamine functions primarily as a precursor for several phosphorylated active forms, which act as coenzymes in metabolic pathways. It reduces intracellular protein glycation by redirecting glycolytic flux and supports the synthesis of nucleic acids necessary for cell survival and proliferation. Additionally, thiamine has been shown to inhibit glucose-induced proliferation of endothelial cells, thus possibly playing a role in the modulation of vascular health.

Pharmacodynamics

Thiamine exhibits antioxidant properties and contributes to erythropoiesis, cognitive function, and mood regulation. It has protective effects against oxidative stress, particularly in neuronal tissues, where deficiency can lead to neuronal death due to increased free radical production. Thiamine also modulates glucose metabolism, influencing smooth muscle cell proliferation and potentially impacting the progression of atherosclerosis.

Pharmacokinetics

Thiamine is rapidly absorbed from the gastrointestinal tract, primarily in the jejunum, and is distributed throughout the body, with higher concentrations found in the liver, heart, and brain. It is excreted in urine, and its half-life is relatively short. The vitamin is converted into active forms within tissues, including thiamine diphosphate (TDP), which is the coenzyme form involved in carbohydrate metabolism. The body does not store significant amounts of thiamine, making regular dietary intake essential.

Adverse effects

• Allergic reactions
• Anaphylaxis (rare)
• Gastrointestinal disturbances

Precautions

• Facilities for treating anaphylaxis should be available when parenteral thiamine is administered
• Use with caution in patients with a history of hypersensitivity to thiamine

Pregnancy

Thiamine crosses the placenta but no adverse effects have been reported. Information regarding high doses is limited.

Breast-feeding

Severely thiamine-deficient mothers should avoid breast-feeding as thiamine is present in breast milk.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Thiamine hydrochloride 20 mg/ml oral solution
• Thiamine hydrochloride 50 mg tablets
• Thiamine hydrochloride 100 mg modified-release tablets
• Thiamine hydrochloride oral suspension

Indications

• Dyspepsia
• Cholesterol management
• Support for liver function
• Digestive aid

Dosage

Children: Refer to specific product guidelines or consult a healthcare professional, as dosages for children should be approached cautiously and based on age and weight.

Adults: Refer to specific product guidelines or consult a healthcare professional, as dosages can vary based on formulation.

Mechanism of action

Artichoke is believed to promote bile production by the liver, which aids in the digestion of fats. The active compound cynarin enhances bile flow, which may improve fat digestion and absorption. Additionally, its antioxidant properties help in safeguarding liver cells from oxidative stress, and its potential diuretic effects may contribute to reduced cholesterol levels.

Pharmacodynamics

Artichoke exhibits various pharmacological effects, including hepatoprotective, cholesterol-lowering, and digestive aid properties. The compounds in artichoke may help in lowering serum cholesterol levels and improving liver function. Its antioxidant activity is attributed to its high polyphenolic content, which can mitigate damage from free radicals.

Pharmacokinetics

Artichoke extracts are typically administered orally and are absorbed in the gastrointestinal tract. The bioavailability of its active compounds can vary based on the formulation and the presence of other dietary components. Metabolism primarily occurs in the liver, where its constituents may undergo conjugation. The excretion of metabolites is primarily via the urine.

Adverse effects

• Allergic reactions
• Gastrointestinal discomfort
• Nausea
• Diarrhea
• Flatulence

Interactions

• May interact with anticoagulants due to potential effects on bile production
• Caution advised when used with medications that affect liver enzymes

Precautions

• Use with caution in patients with gallbladder disease
• Caution in patients with allergies to plants in the Asteraceae family

Pregnancy

Insufficient data on safety in pregnancy; consult healthcare provider before use.

Breast-feeding

Limited data available; consult healthcare provider before use.

Storage

Store in a cool, dry place, away from direct sunlight.

Formulations

• Dried leaf extract
• Capsules
• Liquid extract
• Tea

Indications

• Supplemental support for exercise performance
• Potential aid in reducing fatigue during physical exertion

Dosage

Children: Refer to the BNF for Children for specific paediatric dosing information.

Adults: Refer to the BNF for specific dosing recommendations.

Mechanism of action

L-aspartate is hypothesized to enhance performance in prolonged and short intensive exercise by sparing muscle glycogen stores and promoting glycogen resynthesis. It serves as a substrate for energy production in the Krebs cycle and stimulates the purine nucleotide cycle, thus potentially influencing energy metabolism during physical activity.

Pharmacodynamics

As a non-essential amino acid, L-aspartate is produced in sufficient quantities under normal physiological conditions. It is a precursor for protein synthesis and plays a role in various metabolic pathways, including those related to energy production and nucleotide synthesis. It is classified as a glycogenic amino acid, contributing to gluconeogenesis and energy metabolism.

Pharmacokinetics

L-aspartate is readily absorbed and utilized by the body, participating in several metabolic pathways, including the Krebs cycle and amino acid metabolism. The exact pharmacokinetic parameters such as half-life, peak plasma concentration, and elimination route are not well characterized in the literature.

Indications

• Herbal medicine
• Aromatherapy
• Culinary uses
• Cosmetic applications
• Traditional medicine

Dosage

Children: Refer to specific herbal or medicinal guidelines for dosage in children, as this varies widely depending on the species and intended use.

Adults: Refer to specific herbal or medicinal guidelines for dosage, as this varies widely depending on the species and intended use.

Mechanism of action

The mechanism of action of flowers varies widely among species and the specific compounds they produce. Many flowers contain phytochemicals that can have pharmacological effects, such as flavonoids, alkaloids, and essential oils. These compounds can interact with biological pathways, modulating processes such as inflammation, oxidative stress, and microbial activity.

Pharmacodynamics

The pharmacodynamics of flower-derived compounds are diverse, often depending on the specific chemical constituents present. For instance, flavonoids found in many flowers may exhibit antioxidant properties, while alkaloids can act on the central nervous system. The effects of these compounds can vary significantly based on dosage, route of administration, and individual patient factors.

Pharmacokinetics

The pharmacokinetics of flower extracts and their active constituents involve absorption, distribution, metabolism, and excretion processes that can differ greatly among various compounds. Generally, compounds are absorbed through the gastrointestinal tract when ingested, with bioavailability affected by factors like solubility and the presence of other food substances. Metabolism typically occurs in the liver, with excretion primarily via urine or feces.

Pregnancy

The use of flowers, particularly those with psychoactive properties, should be approached with caution during pregnancy due to potential risks to fetal development.

Breast-feeding

Due to limited data on the transfer of flower constituents into breast milk, caution is advised. It is recommended to consult a healthcare professional before use.

Storage

Store in a cool, dry place away from direct sunlight. Ensure that products are kept out of reach of children.

Indications

• Anxiety
• Insomnia
• Restlessness
• Digestive disorders
• Menopausal symptoms

Dosage

Children: Refer to established herbal guidelines or consult a healthcare professional as pediatric dosing is not well defined.

Adults: Refer to established herbal guidelines or consult a healthcare professional for appropriate dosing as it varies widely based on formulation and individual needs.

Mechanism of action

The active constituents of hops, including alpha acids (such as humulone) and beta acids (such as lupulone), exert their effects primarily through modulation of the GABAergic system, which promotes sedation and relaxation. Hops also exhibit anti-inflammatory properties by inhibiting the production of pro-inflammatory cytokines and may possess estrogenic activity through interaction with estrogen receptors.

Pharmacodynamics

Hops demonstrate a range of pharmacodynamic effects, including anxiolytic and sedative actions due to their interaction with the GABA receptor system. The bitter compounds in hops can also stimulate appetite and digestive secretions. Additionally, hops may exert antioxidant effects, guarding against cellular damage caused by oxidative stress.

Pharmacokinetics

The pharmacokinetics of hops are not well-characterized, but studies suggest that the bioactive compounds are absorbed in the gastrointestinal tract, with varying degrees of metabolism in the liver. The half-life of hops constituents is not precisely defined and can depend on the specific compound and its formulation.

Adverse effects

• Drowsiness
• Allergic reactions
• Gastrointestinal disturbances
• Hormonal effects

Interactions

• May enhance the sedative effects of CNS depressants
• Possibly interacts with estrogenic drugs due to its phytoestrogen content

Precautions

• Use with caution in individuals with hormone-sensitive conditions
• Monitor for excessive sedation when combined with other CNS depressants

Pregnancy

Hops should be used with caution during pregnancy due to limited safety data and potential hormonal effects.

Breast-feeding

Not enough reliable information is available; use with caution and consult a healthcare professional.

Storage

Store in a cool, dry place away from direct sunlight.

Formulations

• Dried hops
• Hops extract
• Hops tea
• Capsules containing hops extract

Indications

• Herpes simplex virus infections
• Lysine deficiency

Dosage

Children: Refer to the BNF for Children for specific dosage recommendations.

Adults: Refer to the BNF for specific dosage recommendations.

Mechanism of action

Lysine inhibits the viral replication of the herpes simplex virus by altering the amino acid ratio in the tissue culture media. A higher concentration of L-lysine compared to L-arginine has been shown to reduce viral growth and cytopathogenicity. Additionally, lysine facilitates calcium absorption from the small intestine and is involved in protein synthesis through its role in the tRNA charging process, linking amino acids to their corresponding tRNA for translation.

Pharmacodynamics

Lysine ensures adequate calcium absorption and is involved in the formation of collagen, essential for bone, cartilage, and connective tissues. It aids in the production of various biological molecules, including antibodies, hormones, and enzymes. Deficiency in lysine can manifest as tiredness, inability to concentrate, irritability, and other health issues.

Pharmacokinetics

Lysine is absorbed in the small intestine and is transported in the bloodstream to various tissues, where it participates in protein synthesis and other metabolic processes. The metabolism of lysine involves its degradation and utilization in various biosynthetic pathways.

Adverse effects

• Gastrointestinal upset
• Diarrhea
• Nausea
• Abdominal pain

Precautions

• Use with caution in individuals with kidney disease
• Consult a healthcare professional before use if pregnant or breastfeeding

Pregnancy

Safety in pregnancy has not been established. Consult a healthcare professional before use.

Breast-feeding

Lysine is generally considered safe in breastfeeding, but consult a healthcare professional before use.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Oral tablet
• Oral capsule
• Powder for oral solution

Indications

• Vitamin B6 deficiency
• Peripheral neuropathy associated with isoniazid therapy
• Supplementation in specific dietary deficiencies

Dosage

Children: Refer to the BNF for Children for specific paediatric dosing guidance.

Adults: Refer to the BNF for specific dosing details, typically 10-50 mg daily for deficiency.

Mechanism of action

Pyridoxine, mainly in its active form pyridoxal 5'-phosphate, is involved in numerous biochemical reactions, including amino acid metabolism, glycogen breakdown, nucleic acid synthesis, and the production of key neurotransmitters. It aids in the synthesis of hemoglobin and sphingolipids, and its deficiency can impair several physiological processes, including immune response and vascular health.

Pharmacodynamics

Pyridoxine is utilized for the prevention and treatment of vitamin B6 deficiency, particularly in individuals undergoing treatment with isoniazid, which can deplete vitamin B6 levels. It may also have beneficial effects on blood pressure and lipid profiles, as studies have shown it can lower both systolic and diastolic blood pressure, inhibit platelet aggregation, and improve cholesterol levels. Additionally, it plays a role in enhancing immune function and protecting endothelial cells from injury.

Pharmacokinetics

Pyridoxine is rapidly absorbed from the gastrointestinal tract. It is transported to tissues where it is phosphorylated to its active form, pyridoxal 5'-phosphate. The vitamin is primarily excreted in urine as pyridoxine and its metabolites. Its half-life varies depending on the individual’s nutritional status and other factors. Adequate dietary intake is essential for maintaining optimal levels in the body.

Pregnancy

Pyridoxine is generally considered safe during pregnancy. However, high doses should be avoided unless specifically prescribed.

Breast-feeding

Pyridoxine is excreted in breast milk, but at normal dietary levels it is considered safe for breastfeeding mothers.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Tablets
• Oral solution
• Injectable form

Dosage

Children: Refer to appropriate clinical guidelines or literature for dosing information as no specific data is available.

Adults: Refer to appropriate clinical guidelines or literature for dosing information as no specific data is available.

Pregnancy

There is limited data on the use of springer during pregnancy. Caution is advised.

Breast-feeding

The effects of springer during breastfeeding are not well studied. Caution is recommended.

Storage

Store in a cool, dry place, away from direct sunlight.

Indications

• Thiamine deficiency
• Wernicke's encephalopathy
• Beriberi
• Alcoholism-related complications
• Certain metabolic disorders

Dosage

Children: Refer to BNF for Children for appropriate dosing information.

Adults: Refer to established clinical guidelines or BNF for specific dosing recommendations.

Mechanism of action

Thiamine is a coenzyme for several important enzymatic reactions, including the pyruvate dehydrogenase complex and alpha-ketoglutarate dehydrogenase. It is essential for converting carbohydrates into energy, facilitating the metabolism of glucose, and maintaining normal nerve function.

Pharmacodynamics

Thiamine deficiency leads to impaired carbohydrate metabolism, which can result in neurological and cardiovascular dysfunction. Supplementation with thiamine helps restore normal metabolic function and can alleviate symptoms associated with deficiency, such as Wernicke's encephalopathy and Beriberi. It also plays a role in the synthesis of neurotransmitters and in maintaining myelin integrity.

Pharmacokinetics

Thiamine is readily absorbed from the gastrointestinal tract, with peak plasma concentrations occurring within 1-2 hours after oral administration. It is distributed throughout the body, primarily in the liver, kidneys, and heart. Thiamine is metabolized in the liver to its active form, thiamine pyrophosphate. It has a biological half-life of about 9-18 days and is excreted primarily in the urine. Excess thiamine is excreted, making toxicity rare.

Adverse effects

• Allergic reactions
• Hypersensitivity reactions
• Gastrointestinal disturbances

Interactions

• May interact with certain diuretics, leading to altered thiamine levels

Precautions

• Use with caution in patients with renal impairment
• Monitor patients with a history of thiamine deficiency

Pregnancy

Thiamine is considered safe during pregnancy, as it is an essential nutrient.

Breast-feeding

Thiamine is excreted in breast milk, but supplementation is generally considered safe for breastfeeding mothers.

Storage

Store in a cool, dry place away from direct sunlight.

Formulations

• Thiamine hydrochloride injection
• Thiamine hydrochloride oral tablets
• Thiamine hydrochloride oral solution

Indications

• Insomnia
• Anxiety disorders
• Stress-related symptoms
• Restlessness
• Muscle tension

Dosage

Children: Refer to a pediatric dosing reference or guidelines, as specific pediatric dosing has not been established.

Adults: Refer to specific guidelines for dosage, as doses can vary based on the formulation and indication.

Mechanism of action

Valerian is thought to exert its effects primarily through modulation of the GABA (gamma-aminobutyric acid) neurotransmitter system. It is believed to increase the levels of GABA in the synaptic cleft, enhancing GABAergic transmission, which results in sedative effects. Additionally, valerian contains various compounds, including valerenic acid, which may influence other neurotransmitter systems and have anti-anxiety properties.

Pharmacodynamics

The pharmacodynamic effects of valerian include sedation, anxiolysis, and muscle relaxation. These effects are most pronounced at doses typically used for therapeutic purposes. The onset of action may vary, with some users reporting effects within an hour, while others may require several days of consistent use. Tolerance can develop with prolonged use, and withdrawal symptoms may occur upon abrupt discontinuation after long-term use.

Pharmacokinetics

Valerian is absorbed from the gastrointestinal tract, with peak plasma concentrations occurring approximately 1-2 hours after oral administration. The bioavailability may be affected by factors such as the preparation method and individual metabolism. Valerian is metabolized in the liver, primarily via phase I reactions, and is excreted through the urine. The half-life of its active components can vary, influencing dosing intervals and duration of action.

Adverse effects

• Headache
• Dizziness
• Gastrointestinal disturbances
• Daytime drowsiness
• Allergic reactions

Interactions

• CNS depressants may enhance sedative effects
• Alcohol may increase sedation
• Benzodiazepines may have additive effects

Precautions

• Use with caution in patients with liver disorders
• Avoid use in children without medical supervision
• Discontinue use if adverse effects occur

Pregnancy

Safety during pregnancy has not been established; use only if clearly needed.

Breast-feeding

Safety during breastfeeding has not been established; use with caution.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Dried root
• Tinctures
• Capsules
• Tablets
• Liquid extracts

Indications

• Vitamin deficiency syndromes (e.g., scurvy for vitamin C deficiency, rickets for vitamin D deficiency)
• Support for immune function
• Antioxidant support
• Bone health maintenance
• Vision health
• Energy metabolism support

Dosage

Children: Refer to the BNF for Children for specific vitamin dosing guidelines, which depend on age and nutritional requirements.

Adults: Refer to specific vitamin guidelines as dosage varies significantly depending on the type of vitamin and individual needs.

Mechanism of action

Vitamins function primarily as coenzymes or precursors for coenzymes in enzymatic reactions. For instance, B vitamins are involved in energy metabolism, while vitamins A, C, D, E, and K support various physiological functions including vision, antioxidant activity, calcium regulation, and blood clotting. Each vitamin has a unique mechanism of action based on its structure and role in the body.

Pharmacodynamics

Vitamins exert their effects at the cellular level, influencing metabolic pathways, gene expression, and immune responses. For example, vitamin D regulates calcium and phosphate homeostasis, while vitamin A is crucial for vision and immune function. Deficiencies in vitamins can lead to a range of disorders, highlighting their importance in maintaining health.

Pharmacokinetics

The pharmacokinetics of vitamins vary widely. Fat-soluble vitamins (A, D, E, and K) are stored in liver and adipose tissues and can be released into circulation as needed. Water-soluble vitamins (B-complex and C) are not stored and must be consumed regularly, with excess amounts excreted in urine. Absorption rates, half-lives, and distribution can also differ based on the specific vitamin and individual metabolic factors.

Interactions

• tretinoin+vitamin: Severe (increases risk of vitamin toxicity)
• retinoids+vitamin: Severe (increases risk of vitamin toxicity)
• retinoids+vitamin: Moderate (increases risk of toxicity)
• carbamazepine+vitamin: Unknown (decreases effects)
• cobicistat+vitamin: Unknown (increases exposure)
• vitamin D substances+digoxin: Unknown (increases risk of toxicity)
• idelalisib+vitamin: Unknown (increases exposure)
• clarithromycin+vitamin: Unknown (increases exposure)

Pregnancy

Consult healthcare professional before use. Vitamin supplementation during pregnancy should be carefully managed to avoid hypervitaminosis.

Breast-feeding

Consult healthcare professional before use. Some vitamins can pass into breast milk and may affect the infant.

Storage

Store in a cool, dry place, away from direct sunlight. Ensure it is kept out of reach of children.

Formulations

• {'name': 'Vitamin A', 'form': 'Capsule', 'strength': '10000 IU'}
• {'name': 'Vitamin D', 'form': 'Tablet', 'strength': '1000 IU'}
• {'name': 'Vitamin E', 'form': 'Softgel', 'strength': '400 IU'}

Mechanism of action

It is thought that the mechanism of action of thiamine on endothelial cells is related to a reduction in intracellular protein glycation by redirecting the glycolytic flux. Thiamine is mainly the transport form of the vitamin, while the active forms are phosphorylated thiamine derivatives. Natural derivatives of thiamine phosphate, such as thiamine monophosphate (ThMP), thiamine diphosphate (ThDP), also sometimes called thiamine pyrophosphate (TPP), thiamine triphosphate (ThTP), and thiamine triphosphate (AThTP), that act as coenzymes in addition to their each unique biological functions. Metabolic control analysis predicts that stimulators of transketolase enzyme synthesis such as thiamin (vitamin B-1) support a high rate of nucleic acid ribose synthesis necessary for tumor cell survival, chemotherapy resistance, and proliferation. Metabolic control analysis also predicts that transketolase inhibitor drugs will have the opposite effect on tumor cells. This may have important implications in the nutrition and future treatment of patients with cancer.

Pharmacodynamics

Thiamine is a vitamin with antioxidant, erythropoietic, cognition-and mood-modulatory, antiatherosclerotic, putative ergogenic, and detoxification activities. Thiamine has been found to protect against lead-induced lipid peroxidation in rat liver and kidney. Thiamine deficiency results in selective neuronal death in animal models. The neuronal death is associated with increased free radical production, suggesting that oxidative stress may play an important early role in brain damage associated with thiamine deficiency. Thiamine plays a key role in intracellular glucose metabolism and it is thought that thiamine inhibits the effect of glucose and insulin on arterial smooth muscle cell proliferation. Inhibition of endothelial cell proliferation may also promote atherosclerosis. Endothelial cells in culture have been found to have a decreased proliferative rate and delayed migration in response to hyperglycemic conditions. Thiamine has been shown to inhibit this effect of glucose on endothelial cells.

Mechanism of action

There are also claims that L-aspartate has ergogenic effects, that it enhances performance in both prolonged exercise and short intensive exercise. It is hypothesized that L-aspartate, especially the potassium magnesium aspartate salt, spares stores of muscle glycogen and/or promotes a faster rate of glycogen resynthesis during exercise. It has also been hypothesized that L-aspartate can enhance short intensive exercise by serving as a substrate for energy production in the Krebs cycle and for stimulating the purine nucleotide cycle.

Pharmacodynamics

L-aspartate is considered a non-essential amino acid, meaning that, under normal physiological conditions, sufficient amounts of the amino acid are synthesized in the body to meet the body's requirements. L-aspartate is formed by the transamination of the Krebs cycle intermediate oxaloacetate. The amino acid serves as a precursor for synthesis of proteins, oligopeptides, purines, pyrimidines, nucleic acids and L-arginine. L-aspartate is a glycogenic amino acid, and it can also promote energy production via its metabolism in the Krebs cycle. These latter activities were the rationale for the claim that supplemental aspartate has an anti-fatigue effect on skeletal muscle, a claim that was never confirmed.

Mechanism of action

Proteins of the herpes simplex virus are rich in L-arginine, and tissue culture studies indicate an enhancing effect on viral replication when the amino acid ratio of L-arginine to lysine is high in the tissue culture media. When the ratio of L-lysine to L-arginine is high, viral replication and the cytopathogenicity of herpes simplex virus have been found to be inhibited. L-lysine may facilitate the absorption of calcium from the small intestine. Amino acids are selected for protein synthesis by binding with transfer RNA (tRNA) in the cell cytoplasm. The information on the amino acid sequence of each individual protein is contained in the sequence of nucleotides in the messenger RNA (mRNA) molecules, which are synthesized in the nucleus from regions of DNA by the process of transcription. The mRNA molecules then interact with various tRNA molecules attached to specific amino acids in the cytoplasm to synthesize the specific protein by linking together individual amino acids; this process, known as translation, is regulated by amino acids (e.g., leucine), and hormones. Which specific proteins are expressed in any particular cell and the relative rates at which the different cellular proteins are synthesized, are determined by the relative abundances of the different mRNAs and the availability of specific tRNA-amino acid combinations, and hence by the rate of transcription and the stability of the messages. From a nutritional and metabolic point of view, it is important to recognize that protein synthesis is a continuing process that takes place in most cells of the body. In a steady state, when neither net growth nor protein loss is occurring, protein synthesis is balanced by an equal amount of protein degradation. The major consequence of inadequate protein intakes, or diets low or lacking in specific indispensable amino acids relative to other amino acids (often termed limiting amino acids), is a shift in this balance so that rates of synthesis of some body proteins decrease while protein degradation continues, thus providing an endogenous source of those amino acids most in need. /Amino acids/ The mechanism of intracellular protein degradation, by which protein is hydrolyzed to free amino acids, is more complex and is not as well characterized at the mechanistic level as that of synthesis. A wide variety of different enzymes that are capable of splitting peptide bonds are present in cells. However, the bulk of cellular proteolysis seems to be shared between two multienzyme systems: the lysosomal and proteasomal systems. The lysosome is a membrane-enclosed vesicle inside the cell that contains a variety of proteolytic enzymes and operates mostly at acid pH. Volumes of the cytoplasm are engulfed (autophagy) and are then subjected to the action of the protease enzymes at high concentration. This system is thought to be relatively unselective in most cases, although it can also degrade specific intracellular proteins. The system is highly regulated by hormones such as insulin and glucocorticoids, and by amino acids. The second system is the ATP-dependent ubiquitin-proteasome system, which is present in the cytoplasm. The first step is to join molecules of ubiquitin, a basic 76-amino acid peptide, to lysine residues in the target protein. Several enzymes are involved in this process, which selectively targets proteins for degradation by a second component, the proteasome. /Amino acids/

Pharmacodynamics

Insures the adequate absorption of calcium; helps form collagen ( which makes up bone cartilage & connective tissues); aids in the production of antibodies, hormones & enzymes. Recent studies have shown that Lysine may be effective against herpes by improving the balance of nutrients that reduce viral growth. A deficiency may result in tiredness, inability to concentrate, irritability, bloodshot eyes, retarded growth, hair loss, anemia & reproductive problems.

Mechanism of action

Vitamin B6 is the collective term for a group of three related compounds, pyridoxine (PN), pyridoxal (PL) and pyridoxamine (PM), and their phosphorylated derivatives, pyridoxine 5'-phosphate (PNP), pyridoxal 5'-phosphate (PLP) and pyridoxamine 5'-phosphate (PMP). Although all six of these compounds should technically be referred to as vitamin B6, the term vitamin B6 is commonly used interchangeably with just one of them, pyridoxine. Vitamin B6, principally in its biologically active coenzyme form pyridoxal 5'-phosphate, is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemogloblin, sphingomyelin and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA).

Pharmacodynamics

Vitamin B6 (pyridoxine) is a water-soluble vitamin used in the prophylaxis and treatment of vitamin B6 deficiency and peripheral neuropathy in those receiving isoniazid (isonicotinic acid hydrazide, INH). Vitamin B6 has been found to lower systolic and diastolic blood pressure in a small group of subjects with essential hypertension. Hypertension is another risk factor for atherosclerosis and coronary heart disease. Another study showed pyridoxine hydrochloride to inhibit ADP- or epinephrine-induced platelet aggregation and to lower total cholesterol levels and increase HDL-cholesterol levels, again in a small group of subjects. Vitamin B6, in the form of pyridoxal 5'-phosphate, was found to protect vascular endothelial cells in culture from injury by activated platelets. Endothelial injury and dysfunction are critical initiating events in the pathogenesis of atherosclerosis. Human studies have demonstrated that vitamin B6 deficiency affects cellular and humoral responses of the immune system. Vitamin B6 deficiency results in altered lymphocyte differentiation and maturation, reduced delayed-type hypersensitivity (DTH) responses, impaired antibody production, decreased lymphocyte proliferation and decreased interleukin (IL)-2 production, among other immunologic activities.