FUTURELIFE HIGH PROTEIN SMART FOOD VANILLA POWDER (Per 100g Vit A/Vit B cmplx/Vit B1/Vit B2/Vit B3/Vit B5/Vit B9/Vit B12/Vit C/Vit D/Vit E/Vit H/Vit K/calcium/chromium/copper/iodine/iron/magnesium/manganese/molybdenum/phosphorus/selenium/zinc/inulin/lecithin/potassium/alanine/arginine 900ug/1.2mg/1.3mg/16mg/5mg/1.7mg/400ug/>2ug/100mg/15ug/15mg/30ug/120ug/520mg/70ug/0.4mg/150ug/18mg/56mg/0.8mg/15ug/247mg/55ug/11mg/500mg/378mg/455mg/1080mg/2060mg/2790mg/880mg/5060mg/1060mg/530mg/40mg/1110mg/1850mg/1090mg/300mg/1230mg/1600mg/1290mg)

Indications

• Selenium deficiency
• Supportive therapy in conditions requiring antioxidant support
• Potential adjunct in cancer prevention strategies

Dosage

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

Adults: Initially 100–500 micrograms daily, adjusted according to response and serum levels.

Mechanism of action

Selenium is metabolized to selenophosphate and selenocysteine, which are essential for the synthesis of selenoproteins. This process involves the incorporation of selenium into proteins through a specialized tRNA that recognizes the RNA sequence UGA, which is facilitated by SECIS structures and SBP-2 proteins. Key selenoproteins, like glutathione peroxidases, help protect cells from oxidative damage, thus playing a significant role in reducing the risk of diseases such as atherosclerosis and certain cancers.

Pharmacodynamics

Selenium is incorporated into various selenoproteins that perform essential functions, including antioxidant activity, redox balance, and regulation of thyroid hormones. Its role in antioxidant defense mechanisms is particularly important for protecting cells against reactive oxygen species (ROS). Selenium supplementation has been linked to improved immune function and potential cancer prevention.

Pharmacokinetics

Selenium is absorbed through the gastrointestinal tract, and its bioavailability can vary based on the source and form of selenium. Once absorbed, it is distributed to various tissues, where it is incorporated into selenoproteins. Selenium is primarily excreted through urine, and its half-life can depend on dietary intake and individual metabolism. Selenium status can be assessed through blood levels of selenoproteins and selenium itself.

Adverse effects

• Nausea
• Anaemia
• Aplastic anaemia
• Skin reactions
• Gastrointestinal disorders

Precautions

• Selenium supplementation should not be given unless there is good evidence of deficiency.
• Use caution in patients with a history of hypersensitivity to selenium or its compounds.

Pregnancy

Limited information is available regarding selenium supplementation during pregnancy. Consult specialist sources for guidance.

Breast-feeding

Limited information is available; the effect of selenium on copper levels in milk is conflicting, and its impact on the infant is unknown.

Storage

After opening, store in a refrigerator (2–8°C).

Formulations

• Tablets (e.g., L-Selenomethionine 200 micrograms, SelenoPrecise 100 micrograms)
• Capsules (e.g., Trientine dihydrochloride 250 mg)
• Injection solutions (e.g., Sodium selenite 50 micrograms per 1 ml)

Indications

• Urea cycle disorders
• Hyperammonaemia types I and II
• Citrullinaemia
• Arginosuccinic aciduria
• Deficiency of N-acetyl glutamate synthetase
• Acute hyperammonaemia in carbamylphosphate synthetase deficiency
• Acute hyperammonaemia in ornithine transcarbamylase deficiency

Dosage

Children: Neonate: 100–300 mg/kg daily in 3–4 divided doses; Child (body-weight up to 40 kg): 6 mg/kg/hour; Child (body-weight 40 kg and above): 4 mg/kg/hour.

Adults: Refer to BNF for specific dosing based on condition; typically administered as 5–50 mg/kg twice daily, adjusted according to plasma ammonia concentration.

Mechanism of action

Arginine serves as a substrate for the synthesis of nitric oxide (NO), a crucial signaling molecule, and contributes to the urea cycle, facilitating the detoxification of ammonia in the liver.

Pharmacodynamics

As a precursor for nitric oxide, arginine plays a vital role in vasodilation and modulating blood flow. It also aids in protein synthesis and supports metabolic processes in the body.

Pharmacokinetics

Arginine is absorbed from the gastrointestinal tract and is distributed throughout the body. It undergoes hepatic metabolism, primarily via the urea cycle, and its half-life is influenced by renal function.

Pregnancy

Use only if clearly needed; consult specialist.

Breast-feeding

Use with caution; benefits should outweigh risks.

Storage

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

Formulations

• L-Arginine 500 mg tablets
• L-Arginine 1 gram tablets
• L-Arginine powder for solution
• L-Arginine 500 mg capsules
• L-Arginine 21% concentrate for solution for infusion

Indications

• Nutritional supplementation
• Support for muscle metabolism
• Enhancement of immune function

Dosage

Children: Refer to the BNF for Children for appropriate paediatric dosing guidelines.

Adults: Refer to the BNF for specific dosing information as it varies based on clinical indications.

Mechanism of action

L-Alanine is synthesized from pyruvate via transamination. It serves as an energy source for muscle cells and is significant in the Alanine-Glucose cycle, where it is converted to glucose in the liver. This process is pivotal for regulating blood sugar levels, especially during extended exercise, when branched-chain amino acids (BCAAs) are used for energy and their nitrogen portions are utilized to form L-Alanine.

Pharmacodynamics

L-Alanine is an important energy source for muscle tissue, the brain, and the central nervous system. It strengthens the immune system by facilitating the production of antibodies and plays a role in the metabolism of sugars and organic acids, which are essential for various physiological functions.

Pharmacokinetics

L-Alanine is readily available in the plasma as a free amino acid. It is involved in several metabolic pathways, including biotin metabolism and tRNA charging. The metabolism of L-Alanine primarily occurs in the liver, where it can be converted into glucose, thus participating in the body's energy homeostasis.

Pregnancy

There are no known specific contraindications for the use of alanine during pregnancy; however, it should be used under medical supervision.

Breast-feeding

There is limited data on the effects of alanine during breastfeeding, and it is advised to consult a healthcare provider before use.

Storage

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

Formulations

• L-Alanine powder
• L-Alanine capsules
• L-Alanine tablets

Indications

• Type 2 diabetes mellitus
• Insulin resistance
• Impaired glucose tolerance
• Metabolic syndrome
• Hyperlipidemia

Dosage

Children: Refer to the BNF for Children for specific dosage recommendations suitable for pediatric patients.

Adults: Refer to the BNF for specific dosage recommendations based on the condition being treated.

Mechanism of action

Chromium enhances insulin signaling by upregulating insulin receptor-mediated pathways. It affects downstream effector molecules after insulin binds to its receptor, leading to the activation of phosphatidylinositol 2-kinase (PI3K) and protein kinase B (Akt). This process promotes the translocation of glucose transporter-4 (Glut4) to the cell membrane, facilitating increased glucose uptake. Additionally, chromium can promote GLUT-4 transporter translocation independently of insulin receptor activity under insulin-resistant conditions and aids in cholesterol efflux by increasing membrane fluidity.

Pharmacodynamics

Trivalent chromium is essential for the glucose tolerance factor, which activates insulin-mediated pathways. It enhances insulin binding to cells, increases the density of insulin receptors, and activates insulin receptor kinase, all of which contribute to improved insulin sensitivity. Chromium deficiency can lead to impaired glucose metabolism, and supplementation can normalize glucose tolerance in individuals exhibiting diabetic-like characteristics due to deficiency.

Pharmacokinetics

Chromium absorption occurs primarily in the intestines, but its bioavailability is influenced by various dietary factors, such as the presence of other minerals and vitamins. The mineral is transported in the bloodstream bound to transferrin and is predominantly stored in the liver, spleen, and bone. The elimination of chromium occurs mainly through urine, with small amounts excreted in feces. The half-life and exact metabolic pathways for chromium can vary based on its form and the individual's nutritional status.

Pregnancy

Chromium is generally considered safe during pregnancy when taken in appropriate amounts, but it is advisable to consult a healthcare provider.

Breast-feeding

Chromium is excreted in breast milk, and while it is deemed safe in moderate amounts, consultation with a healthcare provider is recommended.

Storage

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

Dosage

Children: Refer to the BNF for Children for appropriate paediatric dosing information, as dosing in children should be determined based on weight, age, and specific clinical scenario.

Adults: Refer to the specific BNF or product information for adult dosing guidelines, as these can vary significantly depending on the formulation and indications.

Mechanism of action

The mechanism of action of cmplx is dependent on its specific active ingredients. Generally, complex formulations may utilize multiple pathways to exert their effects, including modulation of neurotransmitter activity, inhibition of enzymes, or alteration of cellular signaling pathways.

Pharmacodynamics

Pharmacodynamics will vary based on the individual components of cmplx. In general, the drug may enhance or inhibit physiological responses through receptor interactions, enzyme modulation, or altering the concentration of certain biochemical mediators in the body. The overall impact will depend on the pharmacological properties of the individual components as well as their interactions.

Pharmacokinetics

The pharmacokinetics of cmplx is contingent upon the specific ingredients used in the formulation. Typically, pharmacokinetic parameters such as absorption, distribution, metabolism, and excretion (ADME) will vary. The bioavailability of each component, half-life, and clearance rate will also influence the overall therapeutic profile of the formulation.

Pregnancy

Consult healthcare provider for risk assessment.

Breast-feeding

Consult healthcare provider for risk assessment.

Storage

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

Indications

• Copper deficiency
• Occipital Horn Syndrome
• Menke's disease
• Contraception (via copper IUD)

Dosage

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

Adults: Refer to the relevant clinical guidelines and BNF for specific dosing information.

Mechanism of action

Copper is absorbed from the gastrointestinal tract via high affinity copper uptake proteins and low affinity copper uptake proteins, likely being reduced to the Cu1+ form prior to transport. Inside enterocytes, it binds to the copper transport protein ATOX1, which facilitates its transport to copper transporting ATPase-1 on the Golgi membrane for incorporation into the Golgi apparatus. Once in systemic circulation, copper binds primarily to ceruloplasmin, albumin, and alpha 2-macroglobulin. It acts as a cofactor in a variety of oxidase enzymes and also influences sperm motility when released from copper IUDs, contributing to its contraceptive effect.

Pharmacodynamics

Copper is essential for the activity of many enzymes and plays a vital role in processes such as iron metabolism, neurotransmitter synthesis, and antioxidant defense. Copper ions, particularly when released from intrauterine devices, have been shown to decrease sperm viability, thereby impacting fertility.

Pharmacokinetics

Copper is absorbed from the gut and is predominantly transported in the plasma bound to proteins such as ceruloplasmin and albumin. The absorption efficiency can vary; however, a significant portion of dietary copper is usually absorbed. The body regulates copper levels through hepatic excretion and storage mechanisms, ensuring homeostasis. Excess copper can lead to toxicity, while deficiency results in various health issues.

Pregnancy

Copper is considered essential during pregnancy, but excessive intake should be avoided due to potential toxicity.

Breast-feeding

Copper is excreted in breast milk, and adequate maternal intake is important for infant development.

Storage

Store in a cool, dry place, away from moisture and heat.

Indications

• Type 2 diabetes mellitus
• Hyperglycemia
• Irritable bowel syndrome
• Constipation
• Dysbiosis

Dosage

Children: Refer to the BNF for Children for appropriate pediatric dosing, as it is not universally established.

Adults: Refer to specific clinical guidelines and local protocols for appropriate dosing, as it may vary based on the condition being treated.

Mechanism of action

Inulin functions primarily as a prebiotic, stimulating the growth of beneficial gut bacteria and enhancing gut health. It may improve insulin sensitivity and glycemic control by modulating gut hormones, leading to increased secretion of glucagon-like peptide-1 (GLP-1), which enhances insulin secretion and decreases glucagon levels. Additionally, it may slow gastric emptying, contributing to a reduction in postprandial blood glucose levels.

Pharmacodynamics

Inulin's pharmacodynamics involve its role in carbohydrate metabolism and its effects on gut microbiota. By promoting the growth of beneficial bacteria, it can lead to improved intestinal barrier function and reduced inflammation. Inulin also aids in the modulation of lipid metabolism, potentially lowering cholesterol levels. Its effects on insulin sensitivity can help improve glycemic control in patients with insulin resistance.

Pharmacokinetics

Inulin is not absorbed in the gastrointestinal tract; it remains intact until it reaches the colon. It is fermented by intestinal bacteria, producing short-chain fatty acids (SCFAs) that may have systemic effects. The fermentation of inulin results in an increase in stool bulk and may improve bowel regularity. The time to reach the colon varies, but fermentation typically begins within 24 hours of ingestion. The elimination route is primarily through feces, as it is not metabolized by human enzymes.

Contra-indications

• Hypoglycemia
• Hypersensitivity to inulin or its components

Adverse effects

• Hypoglycemia
• Allergic reactions including rash, itching, or swelling
• Gastrointestinal disturbances such as nausea, vomiting, or diarrhea
• Injection site reactions

Interactions

• Insulin and other antidiabetic agents may increase the risk of hypoglycemia
• Certain medications like corticosteroids, diuretics, and thiazide diuretics may reduce the effectiveness of inulin

Precautions

• Monitor blood glucose levels closely, especially when initiating therapy or adjusting doses
• Caution in patients with renal impairment as clearance may be affected
• Use with caution in patients with liver dysfunction

Pregnancy

Inulin is generally considered safe during pregnancy; however, blood glucose levels should be monitored closely.

Breast-feeding

Inulin is excreted in breast milk, but it is typically considered safe during breastfeeding; consult with a healthcare provider for individualized advice.

Storage

Store in a refrigerator (2-8°C). Do not freeze. Keep out of reach of children.

Formulations

• Injectable forms (e.g., insulin syringes or pens)
• Inhalable formulations (in some regions)

Indications

• Iodine deficiency
• Goiter
• Hypothyroidism
• Thyroiditis
• Fibrocystic breast disease

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines based on age and weight.

Adults: Refer to the BNF for appropriate dosing guidelines based on condition and clinical judgment.

Mechanism of action

Molecular iodine inhibits the induction and promotion of carcinogenesis in mammary tissues and has shown beneficial effects in fibrocystic breast disease. It temporarily decreases thyroid hormone production through the acute Wolff-Chaikoff effect, followed by a return to normal hormone synthesis due to down regulation of the sodium-iodide symport. This mechanism can lead to a transient hypothyroid state in some individuals with underlying thyroid conditions.

Pharmacodynamics

Iodine is vital for the synthesis of thyroid hormones thyroxine (T4) and triiodothyronine (T3). It affects the metabolism of amine-derived hormones and plays a role in amino acid metabolism. The acute excess of iodide can lead to decreased circulating levels of T4 and T3 in susceptible individuals, while most people can escape this effect and maintain normal thyroid function.

Pharmacokinetics

Iodine is absorbed primarily in the gastrointestinal tract and is distributed throughout the body, particularly in the thyroid gland, where it is concentrated for hormone synthesis. The kidney plays a significant role in the excretion of excess iodine. The half-life of iodine in the body varies and can be influenced by dietary intake and underlying health conditions.

Adverse effects

• Hypothyroidism
• Hyperthyroidism
• Iodine allergy
• Gastrointestinal disturbances

Interactions

• Thyroid hormones
• Antithyroid drugs
• Lithium
• Diuretics

Precautions

• Use with caution in patients with thyroid dysfunction
• Monitor thyroid function periodically during treatment
• Pregnant or breastfeeding women should consult a healthcare provider before use

Pregnancy

Iodine is essential for fetal thyroid hormone synthesis, but excessive iodine intake should be avoided.

Breast-feeding

Iodine is excreted in breast milk; consult a healthcare provider regarding supplementation.

Storage

Store in a cool, dry place away from light.

Formulations

• Iodine solution
• Iodine tincture
• Potassium iodide tablets

Indications

• Cholesterol management
• Cognitive support
• Liver health
• Emulsification in food products

Dosage

Children: Refer to the BNF for Children for specific dosing information as it may vary based on the formulation and indication.

Adults: Refer to the BNF for specific dosing information as it may vary based on the formulation and indication.

Mechanism of action

Lecithin serves as a source of phosphatidylcholine, a key component of cell membranes. It facilitates the transport of fats and cholesterol in the body, enhancing lipid metabolism. Additionally, phosphatidylcholine is involved in the synthesis of acetylcholine, a neurotransmitter important for memory and muscle function.

Pharmacodynamics

Lecithin has been shown to influence lipid metabolism, potentially lowering serum cholesterol levels and improving liver function. By serving as an emulsifying agent, it helps to increase the bioavailability of fat-soluble vitamins and other nutrients. Its role in cell membrane integrity supports overall cellular function and health.

Pharmacokinetics

Lecithin is absorbed in the gastrointestinal tract and metabolized in the liver. It is distributed throughout the body, where it is incorporated into cell membranes. The half-life of lecithin is not well-defined due to its nature as a dietary compound, but its components, such as phosphatidylcholine, are rapidly utilized by the body.

Pregnancy

Lecithin may be used during pregnancy, but it is essential to consult a healthcare provider before use.

Breast-feeding

Lecithin is generally considered safe while breastfeeding; however, it is advisable to seek medical advice.

Storage

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

Indications

• Manganese deficiency
• Bone health and development
• Antioxidant support
• Enzyme cofactor in metabolic processes

Dosage

Children: Refer to the BNF for Children for appropriate dosing recommendations.

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

Mechanism of action

Manganese serves as a cofactor for several enzymes, including manganese superoxide dismutase (MnSOD), which protects cells from oxidative stress by catalyzing the dismutation of superoxide radicals into oxygen and hydrogen peroxide. It also participates in the activation of enzymes involved in carbohydrate, fat, and protein metabolism.

Pharmacodynamics

Manganese plays a role in various biochemical pathways, particularly in the metabolism of amino acids, cholesterol, glucose, and carbohydrates. It is crucial for bone formation and the maintenance of cartilage. Manganese also aids in the synthesis of glycosyltransferases, which are important for the formation of glycoproteins and proteoglycans.

Pharmacokinetics

Manganese is absorbed primarily in the small intestine, with absorption efficiency influenced by dietary factors and the presence of competing minerals. It is transported in the bloodstream bound to proteins such as alpha-2-macroglobulin and transferrin. Manganese is stored in the liver, pancreas, and bones, and is excreted primarily through bile and to a lesser extent in urine. Its half-life in the human body is not well defined due to its trace nature and variable absorption.

Pregnancy

Manganese is classified as a dietary mineral that is essential for human health, but excessive intake should be avoided during pregnancy as it may affect fetal development.

Breast-feeding

Manganese is present in breast milk, and normal dietary intake is considered safe during breastfeeding. However, excessive supplementation should be avoided.

Storage

Store in a cool, dry place, away from direct light and moisture.

Indications

• Molybdenum deficiency
• Support for enzymatic functions related to sulfur metabolism
• Potential use in metabolic disorders associated with sulfite toxicity

Dosage

Children: Refer to specific guidelines for dosing, as molybdenum is typically obtained from dietary sources and supplementation is uncommon.

Adults: Refer to specific guidelines for dosing, as molybdenum is typically obtained from dietary sources and supplementation is uncommon.

Mechanism of action

Molybdenum serves as a cofactor for several important enzymes, including sulfite oxidase, which converts sulfite to sulfate, and xanthine oxidase, which is involved in purine metabolism. These enzymatic reactions are crucial for the detoxification of sulfites and the metabolism of nitrogenous compounds.

Pharmacodynamics

Molybdenum is vital for the activity of enzymes that contribute to the metabolism of sulfur-containing amino acids, purine degradation, and the detoxification of harmful compounds. Its deficiency can lead to metabolic disorders, highlighting its importance in enzymatic processes within the body.

Pharmacokinetics

Molybdenum is absorbed mainly in the small intestine, and its absorption may be influenced by dietary factors. Once absorbed, it is distributed throughout the body and is predominantly found in the liver, kidneys, and bones. The half-life of molybdenum and its excretion primarily through the urine is not well characterized, but excess amounts are generally eliminated by the body.

Pregnancy

Molybdenum is an essential trace element required for normal human metabolism. Adequate intake during pregnancy is important, but excessive amounts may be harmful. Consultation with a healthcare provider is advised.

Breast-feeding

Molybdenum is secreted in breast milk, and adequate intake is important for the nursing infant. Mothers should ensure they meet recommended dietary allowances.

Storage

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

Indications

• Phosphorus deficiency
• Bone health maintenance
• Nutritional supplementation
• Metabolic bone diseases

Dosage

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

Adults: Refer to the BNF for specific dosing information.

Mechanism of action

Phosphorus decreases the absorption of intercellular calcified cartilage matrix by osteoclasts in the metaphyseal region of growing bones. This results in the formation of 'phosphorus bands' of increased bone density and thickness. Additionally, exposure to white phosphorus impairs protein synthesis by damaging the rough and smooth endoplasmic reticulum, leading to an accumulation of triglycerides in the liver and resulting in hepatic steatosis and fibrosis.

Pharmacodynamics

Phosphorus is vital for the formation of hydroxyapatite in bone, which is necessary for maintaining bone density and strength. It also plays a significant role in energy transfer through ATP and in cellular signaling pathways. The balance of phosphorus in the body is tightly regulated, as both deficiency and excess can lead to serious health issues, including bone disorders and metabolic dysfunctions.

Pharmacokinetics

Phosphorus is absorbed primarily in the intestines, with bioavailability influenced by dietary factors. It is distributed throughout the body and is predominantly found in bones and teeth. Phosphorus is excreted mainly via the kidneys, with regulation occurring through various hormonal mechanisms, including parathyroid hormone and calcitriol. The half-life can vary depending on dietary intake and individual metabolism.

Pregnancy

Phosphorus is generally regarded as safe during pregnancy when consumed in appropriate dietary amounts. However, excessive phosphorus intake should be avoided as it may lead to complications.

Breast-feeding

Phosphorus is excreted in breast milk, but it is essential for the health of both the mother and the infant. Supplementation should be considered carefully.

Storage

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

Mechanism of action

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.

Pharmacodynamics

Studies have shown that is has improved immune responses to bacteria, viruses and tumor cells; promotes wound healing and regeneration of the liver; causes the release of growth hormones; considered crucial for optimal muscle growth and tissue repair.

Mechanism of action

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. Converging data from epidemiological, ecological, and clinical studies have shown that selenium (Se) can decrease the risk for some types of human cancers. Induction of apoptosis is considered an important cellular event that can account for the cancer preventive effects of Se. Prior to occurrence of apoptosis, Se compounds alter the expression and/or activities of signaling molecules, mitochondria-associated factors, transcriptional factors, tumor suppressor genes, and cellular reduced glutathione. Mechanistic studies have demonstrated that the methylselenol metabolite pool has many desirable attributes of chemoprevention, whereas the hydrogen selenide pool with excess of selenoprotein synthesis can lead to DNA single-strand breaks. To elucidate the effects of Se on cytotoxic events, it should be remembered that the chemical forms and the dose of Se, and the experimental system used, are determinants of its biological activities. This mini-review focuses on elucidation of the molecular mechanisms of cancer prevention by Se with the apoptotic approach. /Selenium/ Selenium status can also influence thyroid hormone function via the deiodinase enzymes. Selenium is a critical component of the deiodinase enzymes, including iodothyronine 5'-deiodinases, which convert the prohormone thyroxine (T4) to the active circulating form, triiodothyronine (T3). Selenium is also a component of GPX, the main enzyme responsible for protecting thyroid cells against oxidative damage. GPX is involved in the detoxification of hydrogen peroxide, which is produced in the thyroid during the conversion of T4 to T3. /Selenium/ Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low in the organism. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenium may have a role in hepatic heme metabolism that is related to GPX or lipid peroxidation. Selenocysteine is specifically found in some proteins (e.g., glutathione peroxidase); selenomethionine appears to randomly substitute for methionine in protein synthesis. This appears to be an additional mechanism for intermediate- or chronic-duration toxicity. Skin, hair, and nail damage are significant indicators of chronic selenium overexposure. The mechanism causing these integumentary effects is unclear, but could be related to the high selenium concentrations in these tissues as a consequence of the substitution of selenium for sulfur in certain amino acids, including the disulfide bridges that pr

Pharmacodynamics

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

Mechanism of action

L-Alanine is a non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. BCAAs are used as a source of energy for muscle cells. During prolonged exercise, BCAAs are released from skeletal muscles and their carbon backbones are used as fuel, while their nitrogen portion is used to form another amino acid, Alanine. Alanine is then converted to Glucose by the liver. This form of energy production is called the Alanine-Glucose cycle, and it plays a major role in maintaining the body's blood sugar balance.

Pharmacodynamics

Is an important source of energy for muscle tissue, the brain and central nervous system; strengthens the immune system by producing antibodies; helps in the metabolism of sugars and organic acids.

Mechanism of action

Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules. Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake. Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt. Under insulin-resistant conditions, chromium also promotes GLUT-4 transporter translocation that is independent of activity of IR, IRS-1, PI3-kinase, or Akt; chromium mediates cholesterol efflux from the membranes via increasing fluidity of the membrane by decreasing the membrane cholesterol and upregulation of sterol regulatory element-binding protein. As a result, intracellular GLUT-4 transporters are stimulated to translocate from intracellular to the plasma membrane, leading to enhanced glucose uptake in muscle cells. Chromium attenuates the activity of PTP-1B _in vitro,_ which is a negative regulator of insulin signaling. It also alleviates ER stress that is observed to be elevated the suppression of insulin signaling. ER stress is thought to activate c-Jun N-terminal kinase (JNK), which subsequently induces serine phosphorylation of IRS and aberration of insulin signalling. Transient upregulation of AMPK by chromium also leads to increased glucose uptake. While the toxicity of metals and metalloids, like arsenic, cadmium, mercury, lead and chromium, is undisputed, the underlying molecular mechanisms are not entirely clear. General consensus holds that proteins are the prime targets; heavy metals interfere with the physiological activity of specific, particularly susceptible proteins, either by forming a complex with functional side chain groups or by displacing essential metal ions in metalloproteins. Recent studies have revealed an additional mode of metal action targeted at proteins in a non-native state; certain heavy metals and metalloids have been found to inhibit the in vitro refolding of chemically denatured proteins, to interfere with protein folding in vivo and to cause aggregation of nascent proteins in living cells. Apparently, unfolded proteins with motile backbone and side chains are considerably more prone to engage in stable, pluridentate metal complexes than native proteins with their well-defined 3D structure. By interfering with the folding process, heavy metal ions and metalloids profoundly affect protein homeostasis and cell viability. This review describes how heavy metals impede protein folding and promote protein aggregation, how cells regulate quality control systems to protect themselves from metal toxicity and how metals might contribute to protein misfolding disorders.

Pharmacodynamics

Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity. In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency.

Mechanism of action

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. The reason for the less severe reaction when the foreign body is at a distance from the retina has been proposed to be ... that near the retina & its blood vessels there is greater oxygen tension than at a distance, which causes metallic copper to oxidize to toxic copper compounds more rapidly close to or in contact with the retina than at a distance. Furthermore, the abscess formation that is characteristic of copper undergoing oxidation close to the retina & choroiod can be attributed to attraction of polymorphonuclear leukocytes from these nearby vascular tissues, which become heavily infiltrated. Liquefaction & disorganization of the vitreous body has been explained on the basis of copper catalysis of oxidation of ascorbic acid, leading to depolymerization of the hyaluronic acid of the vitreous humor. Changes in protein & hexosamine content have also been related to decrease in viscosity of the vitreous humor. Increased content of amino acids in the vitreous humor has been consistent with proteolysis of the vitreous body, but decreased concentration in the aqueous humor has suggested suppression of secretion of amino acids by the ciliary body under the influence of copper.

Pharmacodynamics

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.

Mechanism of action

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. An acute iodide excess (above the preexisting dietary intake) transiently decreases the production of thyroid hormones in the thyroid gland; this is referred to as the acute Wolff-Chaikoff effect. In normal people, this is followed by a return to normal levels of hormone synthesis, referred to as escape from the acute Wolff-Chaikoff effect, without a significant change in circulating hormone levels. Escape is thought to be the result of down regulation of the sodium-iodide symport (NIS), the iodide transporter in the thyroid gland, resulting in a decrease in the intrathyroidal iodine and the resumption of normal hormone synthesis. An acute or chronic excess of iodide can also decrease circulating T4 and T3 levels and induce a hypothyroid state in some people who have underlying thyroid disorders. These effects are the result of a failure to escape from the acute Wolff-Chaikoff effect. Most people who experience iodine-induced hypothyroidism recover when the excess iodine intake is discontinued.

Mechanism of action

Phosphorus apparently decreases the absorption of intercellular calcified cartilage matrix by osteoclasts, in the metaphyseal region of growing bones. Administration of phosphorus to growing animals or children produces "phosphorus bands" of increased bone density and thickness that are visible grossly or from radiograms. The "phosphorus bands" are observed in the metaphyseal region of growing bones, and represent areas of decreased absorption of the calcified cartilage matrix. Exposure to white phosphorus has been shown to damage the rough endoplasmic reticulum and cause a disaggregation of polyribosomes. This damage results in impairment of protein synthesis, in particular, a decrease in the synthesis of the apolipoprotein portion of very low density lipoproteins (VLDL), which are required for the transport of triglycerides. A significant decrease in protein synthesis has been detected as early as 3 hours after oral exposure. The smooth endoplasmic reticulum is also involved in the formation of the VLDLs, and damage to the smooth endoplasmic reticulum also impairs the formation of VLDLs. The net result of these ultrastructural changes is an accumulation of triglycerides in the liver. This results in steatosis and fibrosis, which is one of the mechanisms involved in the hepatotoxicity of white phosphorus. The mechanism behind the damage to the endoplasmic reticulum is not known; also, it is not known whether white phosphorus itself or a metabolite of white phosphorus is the damaging agent. In addition to these damages, white phosphorus or a metabolite causes damage to the mitochondria and nuclei in the livers of animals orally exposed to white phosphorus. The damage to the mitochondria may impair the cell's ability to produce ATP, thus resulting in necrosis of the cell. Fatty infiltration and/or cellular damage has also been observed in the kidney, brain, and heart. It is possible that white phosphorus (or a metabolite) also impairs the ability of cells in these organs to produce ATP. The mitochondrial damage may also inhibit fatty acid oxidation (also contributing to the decreased availability of ATP) which could result in an accumulation of fat in the organs.