NUCEPTION TABLET (Each film coated Tablet contains Vit C/Vit D3/Vit E/Vit B1/Vit B2/Vit B3/Vit B6/Vit B9/Vit B12/Iron/Zinc/Selenium/Chromium/Magnesium/L-Arginine/CoQ10/Inositol/Chaste Berry Extract/D-Chiro-Inositol/Grape Seed Extract/Alpha Lipoic Acid 45mg/300iu/2mg/4mg/2.5mg/10mg/5mg/200mcg/10mcg/7mg/7.5mg/25mcg/30mcg/30mg/50mg/2.5mg/25mg/28mg/25mg/25mg/25mg)

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

• Hypertension
• Benign prostatic hyperplasia
• Urinary retention related to prostate enlargement

Dosage

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

Adults: Refer to the BNF for specific dosing recommendations based on individual clinical scenarios.

Mechanism of action

Alpha acts by selectively blocking alpha-1 adrenergic receptors, which are responsible for mediating vasoconstriction in blood vessels. By inhibiting these receptors, alpha promotes vasodilation, leading to a decrease in peripheral vascular resistance and subsequently lowering blood pressure. Additionally, this action can help alleviate urinary symptoms associated with an enlarged prostate.

Pharmacodynamics

The pharmacodynamics of alpha involve its competitive antagonism at alpha-1 adrenergic receptors, resulting in decreased vasoconstriction and increased blood flow. This mechanism is beneficial in conditions characterized by high blood pressure and urinary retention due to prostatic enlargement. The onset of action typically occurs within hours, with peak effects observed within a few days of consistent dosing.

Pharmacokinetics

Alpha is absorbed well from the gastrointestinal tract, with peak plasma concentrations achieved within 1-3 hours post-administration. The drug undergoes hepatic metabolism, primarily via cytochrome P450 enzymes, resulting in active and inactive metabolites. The elimination half-life varies, but it generally is around 6-12 hours, allowing for once-daily dosing in many cases. Renal excretion is a significant route for its metabolites, necessitating caution in patients with renal impairment.

Interactions

• maois, irreversible + alpha blockers: Severe (increases effects)
• ribociclib + alpha blockers: Severe (increases exposure)
• cobicistat + alpha blockers: Moderate (increases exposure)
• idelalisib + alpha blockers: Moderate (increases exposure)
• dronedarone + alpha blockers: Unknown (increases exposure)
• antifungals, azoles + alpha blockers: Unknown (increases exposure)
• crizotinib + alpha blockers: Unknown (increases exposure)
• imatinib + alpha blockers: Unknown (increases exposure)
• letermovir + alpha blockers: Unknown (increases exposure)
• clarithromycin + alpha blockers: Unknown (increases exposure)

Indications

• Antioxidant support
• Anti-inflammatory effects
• Cardiovascular health
• Cognitive function enhancement
• Support in weight management
• Blood sugar regulation

Dosage

Children: Refer to established dietary guidelines or recommendations for berry consumption in children, as no specific dose has been established for medicinal use.

Adults: Refer to established dietary guidelines or recommendations for berry consumption, as no specific dose has been established for medicinal use.

Mechanism of action

Berries exert their beneficial effects primarily through their high antioxidant capacity, primarily due to compounds such as anthocyanins, flavonoids, and vitamin C. These compounds help reduce oxidative stress and inflammation in the body. Additionally, the fiber content in berries aids in digestion and contributes to the regulation of blood glucose levels.

Pharmacodynamics

The pharmacodynamic effects of berries include antioxidant activity, anti-inflammatory properties, and modulation of metabolic processes. Their consumption has been associated with improved cardiovascular health, cognitive function, and reduced risk of chronic diseases such as diabetes and obesity. The bioactive compounds in berries may enhance endothelial function, improve insulin sensitivity, and influence lipid metabolism.

Pharmacokinetics

The pharmacokinetics of berry compounds vary depending on the specific type and chemical structure of the bioactive constituents. Generally, after ingestion, flavonoids and other polyphenols are absorbed in the gastrointestinal tract, undergo metabolism in the liver, and are then distributed throughout the body. The bioavailability of these compounds can be influenced by the presence of other food components, individual metabolism, and the specific berry consumed.

Pregnancy

The safety of berry consumption during pregnancy varies by type; consult a healthcare professional for specific advice.

Breast-feeding

Generally considered safe, but specific berries should be discussed with a healthcare provider.

Storage

Store in a cool, dry place, away from direct sunlight. Fresh berries should be refrigerated.

Indications

• Premenstrual syndrome (PMS)
• Menstrual irregularities
• Menopause symptoms
• Polycystic ovary syndrome (PCOS)
• Fertility enhancement

Dosage

Children: Safety and efficacy in children have not been established; consult a healthcare provider for guidance.

Adults: Refer to herbal product guidelines, as specific dosing can vary widely based on formulation and concentration.

Mechanism of action

Chasteberry acts on the hypothalamus and pituitary gland to modulate the secretion of hormones. It is thought to increase the production of luteinizing hormone (LH) and decrease the production of follicle-stimulating hormone (FSH), which may help balance estrogen and progesterone levels. Its active compounds, such as flavonoids and terpenoids, may also influence dopamine receptors, leading to a reduction in prolactin levels, which can help alleviate symptoms of PMS and other menstrual disorders.

Pharmacodynamics

Chasteberry exhibits its pharmacological effects primarily through modulation of the endocrine system, particularly by influencing the hypothalamic-pituitary-gonadal axis. Its ability to decrease prolactin levels can help in conditions where high prolactin is a contributing factor, such as in amenorrhea or galactorrhea. Additionally, it may have mild anti-inflammatory and antioxidant properties.

Pharmacokinetics

The pharmacokinetics of chasteberry are not fully characterized. However, it is generally believed that its active constituents are absorbed through the gastrointestinal tract and can exert systemic effects. The onset of action may take several weeks of consistent use, and the metabolism and excretion pathways are largely unstudied, making it difficult to provide detailed pharmacokinetic parameters.

Adverse effects

• Gastrointestinal disturbances
• Headache
• Rash
• Dizziness
• Fatigue

Interactions

• May interact with hormone-sensitive conditions due to its dopaminergic properties
• Potential interaction with oral contraceptives and hormone replacement therapy

Precautions

• Use with caution in individuals with hormone-sensitive conditions
• Monitor for potential side effects in patients with a history of hormonal disorders

Pregnancy

Chaste tree should be avoided during pregnancy due to its effects on hormonal balance.

Breast-feeding

Due to limited safety data, chaste tree is not recommended during breastfeeding.

Storage

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

Formulations

• Dried fruit
• Tincture
• Capsules
• Extracts

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.

Indications

• Heart failure
• Hypertension
• Statin myopathy
• Cancer

Dosage

Children: Refer to BNF for Children for specific dosing information in paediatric patients.

Adults: Refer to BNF for specific dosing information based on the clinical condition being treated.

Mechanism of action

Ubidecarenone is an essential cofactor in the mitochondrial electron transport chain. Its primary functions include the acceptance of electrons from complexes I and II, which is vital for ATP production. Additionally, it acts as a mobile redox agent, shuttling electrons and protons in the electron transport chain. Ubidecarenone also provides antioxidant activity in mitochondria and cellular membranes, protecting against lipid peroxidation and inhibiting the oxidation of LDL-cholesterol.

Pharmacodynamics

Ubidecarenone has roles in various physiological processes, including sulfide oxidation, regulation of the mitochondrial permeability transition pore, and the translocation of protons and calcium ions across biological membranes. Research indicates its potential benefits in treating conditions such as cancer, statin myopathy, congestive heart failure, and hypertension.

Pharmacokinetics

Coenzyme Q10 is absorbed in the small intestine, with bioavailability affected by dietary fats. Once absorbed, it is distributed throughout body tissues, particularly in the heart, liver, and kidneys. The half-life of CoQ10 is approximately 33 hours, and it is metabolized primarily in the liver. Excretion occurs mainly through the bile and urine.

Pregnancy

There is insufficient evidence regarding the safety of CoQ10 during pregnancy. Consult a healthcare professional before use.

Breast-feeding

Limited data suggests that CoQ10 is likely safe during breastfeeding, but consult a healthcare professional for personalized advice.

Storage

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

Formulations

• Capsules
• Tablets
• Soft gels

Indications

• Insulin resistance
• Polycystic ovary syndrome (PCOS)
• Metabolic syndrome
• Type 2 diabetes

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines.

Mechanism of action

D-chiro-inositol enhances insulin sensitivity and plays a role in glucose metabolism by acting as a secondary messenger in insulin signaling. It participates in the phosphoinositide signaling pathway, which is crucial for the action of insulin on glucose uptake in muscle and fat tissues. Furthermore, it is involved in the biosynthesis of inositol phosphates, which are important for cellular signaling.

Pharmacodynamics

D-chiro-inositol has been shown to improve insulin sensitivity, reduce insulin resistance, and assist in the regulation of ovarian function in women with PCOS. It is thought to modulate the insulin signaling pathway, thereby improving metabolic parameters associated with insulin resistance. Additionally, it may influence lipid metabolism and reduce triglyceride levels.

Pharmacokinetics

The pharmacokinetics of D-chiro-inositol, including its absorption, distribution, metabolism, and excretion, are not extensively characterized. It is generally considered to be well-absorbed when administered orally. D-chiro-inositol is thought to be metabolized in the liver, and its elimination half-life is not well-established. Further studies are needed to detail its pharmacokinetic profile.

Pregnancy

There is insufficient data on the use of d-chiro-inositol in pregnancy. Caution is advised and it should only be used if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Limited data is available on the excretion of d-chiro-inositol in human milk. Caution is recommended when administering to breastfeeding mothers.

Storage

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

Indications

• General wellness support
• Anti-inflammatory effects
• Antioxidant activity
• Digestive aid
• Support for immune function

Dosage

Children: Paediatric dosing should be determined based on the specific extract and its intended use. Consultation with a healthcare provider is recommended for accurate dosing.

Adults: Dosage varies widely depending on the specific extract and formulation. It is essential to follow the manufacturer's instructions or consult a healthcare professional for appropriate dosing.

Mechanism of action

The mechanism of action of herbal extracts can vary significantly based on their constituents. Commonly, they exert their effects through multiple pathways including modulation of neurotransmitter systems, interference with inflammatory processes, or direct antioxidant activity. Some extracts may activate certain receptors or inhibit enzymes related to disease processes.

Pharmacodynamics

The pharmacodynamics of extracts is complex due to the presence of multiple active compounds which can have synergistic or antagonistic effects. These compounds may influence cellular signaling pathways, alter gene expression, or modulate immune response. The overall pharmacological profile is determined by the specific composition of the extract, its concentration, and the biological target it interacts with.

Pharmacokinetics

The pharmacokinetics of extracts involves absorption, distribution, metabolism, and excretion of the active compounds. Generally, herbal extracts are absorbed in the gastrointestinal tract, with bioavailability influenced by factors such as formulation, the presence of food, and individual metabolic differences. Compounds may undergo hepatic metabolism, and elimination can occur through urine or feces, depending on their chemical nature.

Pregnancy

Consult a healthcare professional before use, as the safety of the extract during pregnancy has not been established.

Breast-feeding

Consult a healthcare professional before use, as the safety of the extract during breastfeeding has not been established.

Storage

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

Dosage

Children: Refer to specific medication guidelines for dosing adjustments due to grapefruit juice interactions.

Adults: Refer to specific medication guidelines for dosing adjustments due to grapefruit juice interactions.

Mechanism of action

Grapefruit juice contains compounds called furanocoumarins, which inhibit cytochrome P450 3A4 (CYP3A4) enzymes in the liver and intestines. This inhibition can lead to increased plasma concentrations of drugs that are metabolized by CYP3A4, resulting in enhanced pharmacological effects and potential toxicity.

Pharmacodynamics

The pharmacodynamic effects of grape juice are closely related to its antioxidant properties, primarily due to resveratrol and flavonoids. These compounds help in reducing oxidative stress and inflammation. However, the primary clinical concern is the modulation of drug metabolism, particularly affecting drugs with a narrow therapeutic index.

Pharmacokinetics

Grapefruit juice can significantly alter the pharmacokinetics of certain medications by affecting their absorption and metabolism. The inhibition of CYP3A4 can lead to increased bioavailability of drugs that are substrates of this enzyme, resulting in higher plasma concentrations. The effects of grapefruit juice can persist for up to 24 hours post-consumption, complicating timing and dosing of affected medications.

Interactions

• grapefruit juice + abemaciclib: Severe (increases exposure)
• grapefruit juice + aliskiren: Severe (decreases exposure)
• grapefruit juice + amiodarone: Severe (increases exposure)
• grapefruit juice + dronedarone: Severe (increases exposure)
• grapefruit juice + rupatadine: Severe (increases exposure)
• grapefruit juice + piperaquine: Severe (increases concentration)
• grapefruit juice + antipsychotics, second generation: Severe (increases exposure)
• grapefruit juice + lurasidone: Severe (increases exposure)
• grapefruit juice + quetiapine: Severe (increases exposure)
• grapefruit juice + cariprazine: Severe (increases exposure)

Pregnancy

Consult healthcare provider for guidance on use during pregnancy.

Breast-feeding

Consult healthcare provider for guidance on use during breastfeeding.

Storage

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

Indications

• Polycystic ovary syndrome (PCOS)
• Generalized anxiety disorder
• Depression
• Obsessive-compulsive disorder
• Insulin resistance

Dosage

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

Adults: Refer to the BNF for specific dosing recommendations, as doses may vary based on the condition being treated.

Mechanism of action

Inositol functions primarily as a precursor for the synthesis of phosphoinositides, which are key components of cell membranes. These phosphoinositides are involved in various intracellular signaling pathways, particularly those mediated by G-protein coupled receptors. Inositol also influences the action of neurotransmitters such as serotonin and has been shown to enhance insulin sensitivity and glucose metabolism.

Pharmacodynamics

Inositol has been observed to have mood-stabilizing effects and may improve insulin sensitivity. Its role in cell signaling impacts various physiological processes, including cellular communication and metabolic regulation. The therapeutic effects of inositol in psychiatric conditions may be attributed to its ability to modulate neurotransmitter systems, particularly involving serotonin and dopamine.

Pharmacokinetics

Inositol is well-absorbed from the gastrointestinal tract, with peak plasma levels occurring within 1 to 2 hours after ingestion. It is distributed throughout the body and can cross the blood-brain barrier. Inositol is predominantly excreted in the urine, with a half-life that varies based on dosage and individual metabolism. Metabolism occurs primarily through dephosphorylation to form various inositol phosphates.

Pregnancy

Inositol is generally considered safe during pregnancy but should be used under medical supervision.

Breast-feeding

Inositol is likely safe during breastfeeding, but consult a healthcare provider for specific recommendations.

Storage

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

Formulations

• Powder
• Capsules

Indications

• Cardiovascular diseases
• Erectile dysfunction
• Peripheral arterial disease
• Wound healing
• Muscle growth and recovery
• Immune system support

Dosage

Children: For paediatric dosing, it is important to refer to the BNF for Children for appropriate guidelines based on the child's age, weight, and clinical condition.

Adults: The typical dosage for adults varies based on the condition being treated, but common oral doses range from 2 to 30 grams per day, divided into multiple doses. For specific dosing recommendations, please refer to the BNF.

Mechanism of action

L-arginine is converted to nitric oxide by nitric oxide synthase (NOS), which is crucial for vascular function and blood flow regulation. NO activates guanylate cyclase, leading to increased levels of cyclic GMP, a secondary messenger that mediates vasodilation and other cellular responses. This pathway is vital in both the cardiovascular and immune systems, with different isoforms of NOS (eNOS, nNOS, iNOS) contributing to various physiological effects.

Pharmacodynamics

L-arginine has been shown to enhance immune responses, improve wound healing, stimulate growth hormone release, and support muscle hypertrophy and tissue repair. Its role in nitric oxide production aids in vasodilation, improving blood circulation and oxygen delivery to tissues, which is essential for recovery and regeneration.

Pharmacokinetics

L-arginine is absorbed from the gastrointestinal tract, with peak plasma concentrations occurring within 1-2 hours after oral administration. It is metabolized primarily in the liver and kidneys, with a half-life of approximately 1-2 hours. The bioavailability of L-arginine can be influenced by dietary intake and metabolic conditions.

Adverse effects

• Gastrointestinal disturbances
• Nausea
• Diarrhea
• Abdominal pain
• Hypotension
• Allergic reactions

Interactions

• Antihypertensive agents may have additive effects leading to increased hypotension
• Sildenafil and other medications for erectile dysfunction may have enhanced effects when used with L-arginine

Precautions

• Caution in patients with a history of asthma or allergies
• Use with caution in patients with hypotension
• Monitor blood pressure in patients taking antihypertensive medications

Pregnancy

The safety of L-arginine in pregnancy has not been established. Consult a healthcare provider before use.

Breast-feeding

L-arginine is excreted in breast milk, and its safety during breastfeeding is not well established. Consult a healthcare provider.

Storage

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

Formulations

• Oral tablets
• Powder for oral solution
• Capsules

Indications

• Diabetic neuropathy
• Oxidative stress-related disorders
• Metabolic syndrome
• Weight management
• Liver health

Dosage

Children: Refer to specific product guidelines, as safety and efficacy in children have not been established.

Adults: Refer to specific product guidelines, as dosages may vary based on the formulation and indication.

Mechanism of action

Lipoic acid acts as a cofactor for mitochondrial enzyme complexes, particularly those involved in the Krebs cycle, enhancing energy production. It also possesses antioxidant properties, neutralizing free radicals and regenerating other antioxidants such as vitamins C and E. Additionally, lipoic acid can modulate various signaling pathways, including those related to insulin sensitivity and inflammation.

Pharmacodynamics

Lipoic acid has a dual role as a coenzyme and an antioxidant. By participating in the decarboxylation of alpha-keto acids, it aids in energy production. Its antioxidant properties contribute to the protection of cells from oxidative stress, which is implicated in various chronic diseases. Lipoic acid can improve insulin sensitivity, making it beneficial in managing glucose metabolism disorders.

Pharmacokinetics

After oral administration, lipoic acid is absorbed in the gastrointestinal tract, with peak plasma concentrations occurring within 30 to 60 minutes. It undergoes hepatic metabolism, primarily via reduction and conjugation, resulting in various metabolites. The elimination half-life is approximately 30 minutes to 2 hours, and it is excreted primarily in urine. The bioavailability of lipoic acid can be affected by food intake.

Adverse effects

• Nausea
• Vomiting
• Abdominal pain
• Skin rash
• Hypoglycemia

Interactions

• May enhance the effects of insulin and other antidiabetic medications
• May interact with heavy metal chelators

Precautions

• Use with caution in patients with diabetes due to the risk of hypoglycemia
• Monitor blood sugar levels in diabetic patients

Pregnancy

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

Breast-feeding

It is not known whether lipoic acid is excreted in human breast milk; caution is advised.

Storage

Store in a cool, dry place away from light.

Formulations

• Capsules
• Tablets
• Injectable solutions

Indications

• Dietary supplement for heart health
• Source of essential fatty acids
• Antioxidant support
• Promotion of digestive health
• Management of cholesterol levels

Dosage

Children: Refer to specific seed type and formulation for dosing information, as it can vary widely based on type and intended use.

Adults: Refer to specific seed type and formulation for dosing information, as it can vary widely based on type and intended use.

Mechanism of action

The bioactive compounds in seeds, such as polyunsaturated fatty acids, phytosterols, and antioxidants, exert various effects in the body. For example, omega-3 fatty acids found in flaxseeds can influence lipid metabolism and reduce inflammation by modulating the production of eicosanoids. Antioxidants such as tocopherols and phenolic compounds can scavenge free radicals, reducing oxidative stress.

Pharmacodynamics

Seeds have shown potential benefits, including the modulation of lipid profiles, reduction in inflammatory markers, and improvement in glycemic control. The consumption of seeds may lead to decreased low-density lipoprotein (LDL) cholesterol levels and increased high-density lipoprotein (HDL) cholesterol levels, contributing to cardiovascular health. The dietary fiber in seeds can also aid in digestive health and promote satiety.

Pharmacokinetics

The pharmacokinetics of seeds can vary widely depending on the type of seed and the specific compounds being analyzed. Generally, the bioactive components are digested and absorbed in the gastrointestinal tract, with fatty acids being incorporated into chylomicrons and transported via the lymphatic system. Antioxidants are absorbed in the small intestine and may have systemic effects, while fiber can influence gastrointestinal motility and fermentation in the colon.

Pregnancy

Consult a healthcare provider before use, as safety during pregnancy is not well established.

Breast-feeding

Consult a healthcare provider before use, as safety during breastfeeding is not well established.

Storage

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

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

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

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.

Pharmacodynamics

Ubidecarenon has roles in many prysiological process including sulfide oxidation, regulation of mitochondrial permeability transition pore and translocation of protons and calcium ions accross biological membranes. Studies have shown its benefitial effect in treating cancer, statin myopathy, congestive heart failure and hypertension.

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.