OPTICARE CAPSULES(Each hard gelatin capsule contains Vitamin C 40mg/ Vitamin E 40iu/ Ext. Beta Carotene 20% 30mg/ Zinc oxide 12.5m/ L-Glutathione 5mg/ Magnesium sulphate 2mg/ Astaxanthin 1% 1mg/ Ext Bilberry 20% 100mg/ Selenium yeast 0.06mg/ Lutein 20% Zeaxanthin 5mg/ Cupric sulphate pentahydrate 2mg)

Indications

• Vitamin C deficiency
• Scurvy
• Adjunct therapy in iron overload conditions

Dosage

Children: Child 1 month–3 years: 125–250 mg daily in 1–2 divided doses; Child 4–11 years: 250–500 mg daily in 1–2 divided doses; Child 12–17 years: 0.5–1 g daily in 1–2 divided doses.

Adults: 500 mg daily, taken in 1-2 divided doses, depending on the clinical condition and dietary needs.

Mechanism of action

Ascorbic acid functions primarily as a reducing agent, facilitating enzymatic reactions in the body, including the hydroxylation of proline and lysine in collagen synthesis. It also plays a role in the absorption of iron from the gastrointestinal tract and enhances the immune response.

Pharmacodynamics

Ascorbic acid is crucial for the maintenance of connective tissue and is involved in the metabolism of several amino acids. Its antioxidant properties help to mitigate oxidative stress and may play a role in reducing the risk of chronic diseases.

Pharmacokinetics

Ascorbic acid is absorbed in the intestines and is widely distributed throughout the body. The renal clearance of ascorbic acid is dose-dependent, with higher doses leading to increased excretion. The half-life varies but is generally around 15 to 30 minutes in healthy individuals, with tissue saturation levels influencing its retention.

Contra-indications

• Hypercalcaemia
• Hyperoxaluria
• Patients with cardiac dysfunction

Adverse effects

• Abdominal pain
• Headache
• Nausea
• Vomiting
• Diarrhoea
• Constipation
• Weight loss
• Polyuria
• Sweating
• Thirst
• Vertigo

Interactions

• Increases risk of cardiovascular adverse effects with iron chelators
• Increases risk of cardiovascular adverse effects with deferiprone
• Increases risk of cardiovascular adverse effects with desferrioxamine

Precautions

• Use with caution in patients with iron overload
• Monitor for symptoms of overdose

Pregnancy

High doses teratogenic in animals but therapeutic doses unlikely to be harmful.

Storage

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

Formulations

• Ascorbic acid 50 mg tablets
• Ascorbic acid 100 mg tablets
• Ascorbic acid 200 mg tablets
• Ascorbic acid 250 mg tablets
• Ascorbic acid 500 mg capsules

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

• Antioxidant support
• Reduction of oxidative stress
• Support for skin health
• Potential benefits in eye health
• Support for cardiovascular health
• Improvement of exercise performance

Dosage

Children: Refer to specific product recommendations and clinical guidelines as there is no established standard dose.

Adults: Refer to specific product recommendations and clinical guidelines as there is no established standard dose.

Mechanism of action

Astaxanthin acts primarily as an antioxidant, neutralizing free radicals and protecting cells from oxidative damage. It is believed to work through various mechanisms, including scavenging reactive oxygen species (ROS) and enhancing the body's natural antioxidant defenses. Astaxanthin may also modulate signaling pathways related to inflammation and immune response.

Pharmacodynamics

Astaxanthin exhibits a high degree of antioxidant activity, being significantly more effective than other carotenoids in quenching singlet oxygen and scavenging free radicals. Its lipophilic nature allows it to integrate into cell membranes, providing cellular protection and stability. This compound may also influence gene expression related to antioxidant enzymes and inflammatory markers, promoting overall cellular health.

Pharmacokinetics

Astaxanthin is absorbed primarily in the intestine, with bioavailability enhanced when taken with fats. Peak plasma concentrations are typically reached within 4 to 6 hours post-ingestion. It is metabolized in the liver and excreted mainly via bile. The elimination half-life of astaxanthin is variable but generally ranges from several hours to a few days, depending on individual metabolism and dosage.

Pregnancy

Astaxanthin is generally considered safe, but there is limited research on its effects during pregnancy. Consult a healthcare provider for guidance.

Breast-feeding

Safety during breastfeeding has not been well established. Consultation with a healthcare provider is recommended.

Storage

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

Indications

• Asthma
• Chronic Obstructive Pulmonary Disease (COPD)
• Hypertension
• Heart Failure
• Cardiac Arrhythmias

Dosage

Children: Refer to the BNF for Children for appropriate dosing

Adults: Refer to the BNF for specific dosing guidelines based on the condition being treated and the formulation of the drug used.

Mechanism of action

Beta-adrenergic agonists stimulate beta-adrenergic receptors, leading to increased intracellular cAMP levels, which causes relaxation of bronchial smooth muscle and dilation of the airways. This mechanism is particularly important in the treatment of asthma and COPD, where airway constriction is a major issue. Beta-blockers, on the other hand, inhibit the effects of catecholamines on beta receptors, resulting in decreased heart rate and myocardial contractility, which is beneficial in managing hypertension and certain types of cardiac arrhythmias.

Pharmacodynamics

The pharmacodynamics of beta drugs vary depending on whether they are agonists or antagonists. Agonists lead to a dose-dependent bronchodilation and increased heart rate, while antagonists decrease heart rate and myocardial oxygen demand. The effects of these drugs can be influenced by patient-specific factors such as receptor sensitivity, presence of comorbid conditions, and concurrent medications.

Pharmacokinetics

The pharmacokinetics of beta drugs can differ substantially. Agonists are typically rapidly absorbed and distributed, with onset of action occurring within minutes. They may have short half-lives, necessitating multiple doses throughout the day. Beta-blockers, in contrast, may have longer half-lives and can be administered once or twice daily. Metabolism usually occurs in the liver, and renal excretion is common for both classes, affecting their dosing in patients with renal impairment.

Interactions

• betablockers, selective + aminophylline: Severe (increases risk of bronchospasm)
• dacomitinib + betablockers, selective: Severe (increases exposure)
• mexiletine + betablockers, selective: Severe (increases risk of cardiovascular adverse effects)
• betablockers, selective + theophylline: Severe (increases risk of bronchospasm)
• beta 2 agonists + linezolid: Severe (increases risk of elevated blood pressure)
• mao-b inhibitors + beta: Severe (increases risk of severe hypertension)
• verapamil + betablockers, non-selective: Severe (increases risk of cardiovascular adverse effects)
• cobicistat + beta: Severe (increases exposure)
• dacomitinib + betablockers, non-selective: Severe (increases exposure)
• idelalisib + beta: Severe (increases exposure)

Indications

• Improvement of visual function
• Support for eye health
• Management of diabetic retinopathy
• Enhancement of microcirculation
• Support for cardiovascular health

Dosage

Children: Consult a healthcare provider for appropriate dosing in children, as specific pediatric dosing may not be established.

Adults: Refer to specific product guidelines or consult a healthcare provider for dosing information, as it can vary based on formulation.

Mechanism of action

Bilberry is thought to exert its effects primarily through the action of anthocyanins, which have been shown to improve visual function and circulation. These compounds may enhance the integrity of the vascular system, inhibit oxidative stress, and improve microcirculation, particularly in the retina, thus potentially aiding in conditions like night blindness and age-related macular degeneration.

Pharmacodynamics

The pharmacodynamic effects of bilberry are largely attributed to its antioxidant properties, which help to scavenge free radicals and reduce oxidative damage in tissues. The anthocyanins in bilberry may also modulate inflammatory responses and improve endothelial function, contributing to better blood flow and reduced risk of cardiovascular complications.

Pharmacokinetics

Bilberry extracts are typically administered orally, and the active constituents are absorbed in the gastrointestinal tract. The bioavailability of anthocyanins can be influenced by factors such as food intake and gastrointestinal pH. Once absorbed, these compounds are metabolized in the liver and excreted primarily through urine. The half-life of bilberry components varies and is influenced by the specific anthocyanins and the formulation used.

Adverse effects

• Gastrointestinal upset
• Allergic reactions
• Headache
• Dizziness

Interactions

• Anticoagulants
• Antiplatelet drugs
• Diabetes medications

Precautions

• Use with caution in individuals with bleeding disorders
• Caution in patients undergoing surgery due to potential bleeding effects

Pregnancy

Bilberry is classified as safe for use during pregnancy, but it should be used under the guidance of a healthcare provider.

Breast-feeding

There is insufficient reliable information regarding the safety of bilberry during breastfeeding, thus caution is advised.

Storage

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

Formulations

• Dried berries
• Powdered extract
• Capsules
• Liquid extract

Indications

• Vitamin A deficiency
• Supplementation for eye health
• Antioxidant support

Dosage

Children: Refer to the BNF for Children for specific dosage recommendations, as they may vary based on the clinical indication and individual patient factors.

Adults: Refer to the BNF for specific dosage recommendations, as they may vary based on the clinical indication and individual patient factors.

Mechanism of action

Carotene acts primarily as a provitamin A, which means it can be converted into retinol (vitamin A) in the body. This conversion occurs in the intestinal mucosa and liver, where carotene is cleaved by the enzyme beta-carotene 15,15'-monooxygenase. The resulting retinol is essential for various biological functions, including the maintenance of vision, epithelial integrity, and reproductive health. Additionally, carotene possesses antioxidant properties, helping to neutralize free radicals and reduce oxidative stress.

Pharmacodynamics

Carotene exhibits its effects through its conversion to vitamin A, which is vital for the maintenance of normal vision, immune function, and cellular health. As an antioxidant, carotene helps protect the body from oxidative stress, which can contribute to chronic diseases such as cancer and cardiovascular disease.

Pharmacokinetics

Carotene is absorbed in the intestine, particularly in the presence of dietary fats, as it is a fat-soluble compound. Once absorbed, it is transported in the bloodstream by lipoproteins and stored in the liver and adipose tissues. The bioavailability of carotene can be influenced by dietary factors, such as the presence of fat and the matrix of the food source. The half-life and metabolism of carotene can vary significantly based on individual factors, including genetics and dietary habits.

Pregnancy

Carotene is generally considered safe during pregnancy, but high doses should be avoided as they may pose risks.

Breast-feeding

Carotene is excreted in breast milk in small amounts and is not known to cause harm to nursing infants.

Storage

Store in a cool, dry place, protected from light.

Formulations

• Capsules
• Tablets
• Liquid preparations

Indications

• Copper deficiency
• Menkes disease
• Wilson disease
• Osteoporosis prevention
• Anemia treatment

Dosage

Children: Refer to established pediatric guidelines for specific dosing based on the condition being treated and individual patient needs.

Adults: Refer to established guidelines for specific dosing based on the condition being treated and individual patient needs.

Mechanism of action

Cupric ions participate in numerous enzymatic reactions as a cofactor. They are involved in the electron transport chain and are essential for oxidative phosphorylation. Copper is known to activate enzymes such as cytochrome c oxidase, which facilitates cellular respiration, and superoxide dismutase, which helps in the detoxification of superoxide radicals, contributing to antioxidant defense mechanisms.

Pharmacodynamics

Cupric has important roles in iron metabolism and the synthesis of collagen and elastin. It contributes to the stabilization of protein structures and assists in the enzymatic functions that protect cells from oxidative stress. The bioavailability of copper is influenced by dietary intake and interactions with other trace elements, notably zinc and iron.

Pharmacokinetics

Cupric is absorbed in the gastrointestinal tract, primarily in the stomach and small intestine. The absorption rate can vary based on dietary factors and the presence of other minerals. Once absorbed, copper is transported in the bloodstream bound to ceruloplasmin and other proteins. It is stored mainly in the liver, brain, and muscles, and is excreted primarily through bile. The half-life of copper in the body is variable, reflecting its dynamic role in metabolism.

Contra-indications

• Hypersensitivity to cupric compounds
• Wilson's disease
• Severe hepatic impairment

Adverse effects

• Gastrointestinal disturbances including nausea and vomiting
• Diarrhea
• Abdominal pain
• Metallic taste
• Kidney damage with excessive doses
• Hepatotoxicity

Interactions

• May reduce the absorption of tetracycline antibiotics
• Ascorbic acid may enhance the absorption of copper
• Zinc and iron may compete with copper for absorption

Precautions

• Use with caution in patients with gastrointestinal disorders
• Monitor liver function in patients receiving high doses
• Assess for signs of copper toxicity, especially with prolonged use

Pregnancy

Copper is an essential trace element and is generally considered safe during pregnancy; however, supplementation should be monitored and tailored to individual needs.

Breast-feeding

Copper is excreted in breast milk, and normal dietary intake is considered safe; excessive supplementation should be avoided.

Storage

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

Formulations

• Copper sulfate
• Copper gluconate
• Copper chloride
• Copper acetate

Mechanism of action

Glutathione (GSH) participates in leukotriene synthesis and acts as a cofactor for the enzyme glutathione peroxidase. It plays a critical role in detoxifying lipophilic toxins through conjugation, enhancing their excretion in bile. Glutathione is involved in detoxifying methylglyoxal, a toxic by-product of metabolism, through the glyoxalase enzyme pathway. Glyoxalase I and II catalyze the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione and then to reduced glutathione and D-lactate. GSH is also a cofactor for conjugation reactions mediated by glutathione S-transferase enzymes and can engage in non-enzymatic conjugation with certain reactive metabolites, such as N-acetyl-p-benzoquinone imine (NAPQI), thereby detoxifying them.

Pharmacodynamics

L-glutathione exerts its antioxidant effects by directly scavenging free radicals and reactive oxygen species, thus preventing cellular damage. It also maintains the activity of other antioxidants, such as vitamins C and E, and plays a crucial role in the regeneration of oxidized glutathione. Due to its involvement in various metabolic pathways, including the detoxification of harmful substances, it is essential for overall cellular health and function.

Pharmacokinetics

L-glutathione is absorbed in the gastrointestinal tract, but its bioavailability is variable due to rapid metabolism and degradation in the intestinal lumen. It is distributed throughout the body, with higher concentrations found in the liver, lungs, and erythrocytes. The metabolism of glutathione primarily occurs in the liver, where it undergoes conjugation and is involved in various metabolic pathways. Excretion occurs mainly through biliary routes, and it is also recycled through the action of enzymes that convert

Pregnancy

There is insufficient data on the safety of glutathione during pregnancy. It is advisable to use it only if clearly needed and after assessing the benefits and risks.

Breast-feeding

Limited information is available regarding the excretion of glutathione in human milk. Caution is advised when administering to breastfeeding women.

Storage

Store in a cool, dry place away from direct sunlight. Ensure the container is tightly closed to maintain product stability.

Indications

• Age-related Macular Degeneration (AMD)
• Cataracts
• Ocular health protection
• Antioxidant support

Dosage

Children: Refer to BNF for Children for specific dosage guidance as it may vary based on formulation and clinical indication.

Adults: Refer to BNF for specific dosage guidance as it may vary based on formulation and clinical indication.

Mechanism of action

Lutein exhibits antioxidant activity by reacting with active oxygen species, leading to the production of biologically active degradation products. It inhibits the peroxidation of membrane phospholipids and reduces lipofuscin formation, which are key contributors to oxidative stress. Additionally, lutein filters blue light and near-ultraviolet radiation, providing protective effects in the retina due to its ability to scavenge reactive oxygen species. It also enhances the expression of connexin-43, facilitating gap junctional communication and offering potential protection against cancer.

Pharmacodynamics

Lutein is concentrated in the macula of the retina, where it exerts protective effects against oxidative stress and high-energy light. Its presence is linked to a decreased risk of developing eye diseases such as Age-related Macular Degeneration (AMD). Studies indicate that higher macular pigment density is associated with a reduced risk of these conditions, highlighting lutein's role in maintaining eye health.

Pharmacokinetics

Lutein is absorbed in the gastrointestinal tract and its bioavailability can be influenced by the presence of dietary fats. It is transported in the bloodstream primarily via lipoproteins and is distributed to various tissues, with a significant accumulation in the retina and lenses of the eyes. The elimination half-life and metabolic pathways are not well characterized, but lutein is known to be more stable against degradation by pro-oxidants compared to other carotenoids.

Pregnancy

Lutein is generally considered safe during pregnancy, but consult a healthcare provider for individual assessment.

Breast-feeding

Lutein is likely safe during breastfeeding, but it is advisable to consult a healthcare provider.

Storage

Store in a cool, dry place away from light.

Formulations

• Supplement capsules
• Softgel formulations
• Powdered forms for mixing

Mechanism of action

Oxides do not have a single mechanism of action as they are a broad category of compounds. However, in general, metal oxides can exhibit catalytic properties, while non-metal oxides may participate in biochemical reactions by forming acids or bases upon dissolution in water.

Pharmacodynamics

The pharmacodynamics of oxides depend on the specific type of oxide and its interaction with biological systems. For instance, metal oxides may have antimicrobial properties, while certain non-metal oxides can influence metabolic pathways through their acid-base chemistry. The effects vary widely, necessitating specific studies for each oxide's role in therapeutic contexts.

Pharmacokinetics

The pharmacokinetics of oxides are also variable. Many metal oxides are poorly soluble and thus have limited absorption when ingested. Non-metal oxides, such as carbon dioxide, can be readily absorbed and utilized in metabolic processes. The distribution, metabolism, and excretion of oxides depend on their chemical form and the biological system in which they are involved.

Pregnancy

Not applicable as oxide is not a drug but a class of chemical compounds.

Breast-feeding

Not applicable as oxide is not a drug but a class of chemical compounds.

Storage

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

Dosage

Children: Refer to the specific drug formulation and clinical guidelines for appropriate dosing. Pediatric doses should be carefully calculated based on the active ingredient and the child's age and weight.

Adults: Refer to the specific drug formulation and clinical guidelines for appropriate dosing. Doses can vary widely based on the active ingredient and its clinical application.

Mechanism of action

Pentahydrate forms do not have a specific mechanism of action, as they are typically salts or hydrates of other active compounds. The effectiveness depends on the active ingredient associated with the pentahydrate form, which may engage in various biochemical interactions in the body to exert therapeutic effects. Generally, the release of the active drug from its hydrated form can influence its absorption and subsequent pharmacological activity.

Pharmacodynamics

The pharmacodynamics of pentahydrate forms is determined by their active ingredients. The hydration state can affect the dissolution rate, which in turn influences the onset of action and overall efficacy. Hydrated forms can improve solubility in biological fluids, leading to enhanced absorption and bioavailability in certain cases. The specific pharmacological action, such as receptor binding or enzyme inhibition, will depend on the drug itself rather than the pentahydrate status.

Pharmacokinetics

The pharmacokinetics of pentahydrate forms is influenced by the solubility and stability of the drug. Generally, a hydrated form may result in increased dissolution rates, promoting better absorption in the gastrointestinal tract. The extent and rate of absorption can vary based on the specific pentahydrate and its active ingredient. Distribution, metabolism, and excretion will depend on the nature of the drug itself, including its half-life and the pathways involved in its elimination from the body.

Pregnancy

Safety in pregnancy has not been established. Use only if the potential benefit justifies the risk.

Breast-feeding

Caution is advised. It is unknown if pentahydrate is excreted in human milk.

Storage

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

Indications

• Hypokalemia
• Potassium depletion
• Certain types of arrhythmias
• Prevention of hypokalemia in patients receiving diuretics

Dosage

Children: Refer to established guidelines or consult the BNF for Children for specific dosing recommendations.

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

Mechanism of action

Potassium ions play a crucial role in cellular physiology. They are essential for maintaining the resting membrane potential of cells and are involved in the generation of action potentials in excitable tissues such as neurons and muscle cells. The influx and efflux of potassium ions across cell membranes are critical for normal cardiac and neuromuscular function.

Pharmacodynamics

Potassium functions as an essential intracellular cation, influencing various physiological processes. It helps regulate heart rhythm, muscle contraction, and nerve impulses. An adequate potassium level is necessary to prevent muscle weakness, paralysis, and arrhythmias. The relationship between potassium levels and these physiological functions is tightly controlled by renal function and dietary intake.

Pharmacokinetics

Potassium is absorbed primarily in the gastrointestinal tract. Following absorption, it is distributed throughout the body's tissues, with approximately 98% of the body's potassium found intracellularly. The kidneys play a critical role in regulating potassium levels by excreting excess potassium in urine. The half-life of potassium in the body can vary significantly based on renal function, dietary intake, and cellular demands.

Pregnancy

There is insufficient data on the safety of pentapotassium during pregnancy. It should only be used if the benefits outweigh the risks.

Breast-feeding

It is not known if pentapotassium is excreted in human milk. Caution is advised when administering to nursing mothers.

Storage

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

Indications

• Prevention of vitamin E deficiency
• Antioxidant therapy
• Support in conditions related to oxidative stress

Dosage

Children: Refer to BNF for Children for specific dosage guidelines.

Adults: Refer to BNF for specific dosage guidelines.

Mechanism of action

Tocopherol acts as a radical scavenger, primarily functioning as an antioxidant for lipid bilayers. It donates hydrogen atoms to free radicals, trapping them and preventing cellular damage. Its effectiveness is influenced by its location within the membrane and its interaction with cytosolic reductants like ascorbate. Tocopherol can trap multiple radicals, including alkyl and peroxy radicals.

Pharmacodynamics

The antioxidant properties of tocopherol lead to significant pharmacodynamic effects, including the inhibition of cell death through modulation of protein kinase C (PKC). Tocopherol also exhibits anti-inflammatory effects, which can be attributed to its influence on cytokines, prostaglandins, prostanoids, and thromboxanes. These interactions may contribute to its protective effects in various pathological conditions.

Pharmacokinetics

Tocopherol is absorbed in the intestines and its bioavailability can be influenced by dietary fat intake. It is transported in the plasma primarily bound to lipoproteins. Tocopherol is stored in adipose tissue and the liver, and its elimination occurs through bile and urine. The half-life of tocopherol can vary depending on the individual's nutritional status and other factors.

Pregnancy

Tocopherol is generally considered safe during pregnancy, but it is advisable to consult a healthcare provider before use.

Breast-feeding

Tocopherol is excreted in breast milk, and while it is considered safe, a healthcare provider should be consulted for specific recommendations.

Storage

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

Indications

• Nutritional supplement
• Support for digestive health
• Enhancement of immune function
• Source of B vitamins

Dosage

Children: Refer to specific product guidelines, as dosage may vary based on formulation and intended use.

Adults: Refer to specific product guidelines, as dosage may vary based on formulation and intended use.

Mechanism of action

Yeast operates through various biochemical pathways, primarily by fermenting sugars to produce alcohol and carbon dioxide. In its role as a dietary supplement, it may enhance gut health by supporting the growth of beneficial gut flora and improving nutrient absorption. Additionally, yeast extract can modulate immune responses and has been studied for its potential antioxidant properties.

Pharmacodynamics

Yeast contains various bioactive compounds, including beta-glucans, which may enhance immune function and exhibit anti-inflammatory properties. The nutrients in yeast, such as B vitamins and amino acids, play crucial roles in metabolic processes, energy production, and overall health maintenance. The fermentation products can also influence gut microbiota composition and enhance digestive health.

Pharmacokinetics

When ingested, yeast components are digested in the gastrointestinal tract where they are broken down into absorbable nutrients. The bioavailability of vitamins and minerals from yeast can vary based on the preparation method. The metabolic byproducts of yeast fermentation are utilized by the body for energy and other metabolic functions. The elimination of yeast components occurs primarily through fecal excretion, as well as through metabolic pathways in the liver.

Adverse effects

• Gastrointestinal discomfort
• Gas and bloating
• Allergic reactions
• Headache

Precautions

• Use with caution in individuals with a compromised immune system
• May cause allergic reactions in sensitive individuals

Pregnancy

Generally considered safe, but consult a healthcare provider before use.

Breast-feeding

Generally considered safe, but consult a healthcare provider before use.

Storage

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

Formulations

• Capsules
• Tablets
• Powder
• Liquid

Indications

• Age-related macular degeneration
• Eye health supplementation
• Antioxidant support

Dosage

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

Adults: Refer to the BNF for specific dosing recommendations.

Mechanism of action

Zeaxanthin acts as a light filter in the retina, protecting the eyes from harmful high-energy light waves like ultraviolet rays. It is believed to neutralize free radicals and reduce oxidative stress, which can contribute to various ocular diseases. Additionally, zeaxanthin is involved in the carotenoid biosynthesis pathways, including its conversion from violaxanthin and its role in various biosynthetic processes.

Pharmacodynamics

Zeaxanthin exhibits antioxidant activity, which helps protect cells from oxidative damage. It is selectively deposited in the macula of the eye, where it contributes to visual acuity and may prevent photochemical damage caused by light exposure. Its presence in the retina aids in filtering blue light and supports overall retinal health.

Pharmacokinetics

Zeaxanthin is absorbed in the gastrointestinal tract after dietary intake, with peak plasma concentrations occurring several hours post-ingestion. It is transported in the bloodstream bound to lipoproteins, and its bioavailability can vary based on dietary fat presence. The half-life of zeaxanthin in the body is not well established but is believed to be several days, as it is stored in the retina and other tissues.

Pregnancy

There is insufficient data on the safety of zeaxanthin during pregnancy. Consult a healthcare provider for advice.

Breast-feeding

Limited data is available on the excretion of zeaxanthin in human milk. Consult a healthcare provider for guidance.

Storage

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

Formulations

• Dietary supplements
• Ophthalmic preparations

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

Glutathione (GSH) participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It also plays a role in the hepatic biotransformation and detoxification process; it acts as a hydrophilic molecule that is added to other lipophilic toxins or wastes prior to entering biliary excretion. It participates in the detoxification of methylglyoxal, a toxic by-product of metabolism, mediated by glyoxalase enzymes. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. GSH is a cofactor of conjugation and reduction reactions that are catalyzed by glutathione S-transferase enzymes expressed in the cytosol, microsomes, and mitochondria. However, it is capable of participating in non-enzymatic conjugation with some chemicals, as it is hypothesized to do to a significant extent with n-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450 reactive metabolite formed by toxic overdose of acetaminophen. Glutathione in this capacity binds to NAPQI as a suicide substrate and in the process detoxifies it, taking the place of cellular protein sulfhydryl groups which would otherwise be toxically adducted. The preferred medical treatment to an overdose of this nature, whose efficacy has been consistently supported in literature, is the administration (usually in atomized form) of N-acetylcysteine, which is used by cells to replace spent GSSG and allow a usable GSH pool.

Mechanism of action

Xanthophylls have antioxidant activity and react with active oxygen species, producing biologically active degradation products. They also can inhibit peroxidation of membrane phospholipids and reduce lipofuscin formation, both of which contribute to their antioxidant properties. Lutein is naturally present in the macula of the human retina. It filters out potentially phototoxic blue light and near-ultraviolet radiation from the macula. The protective effect is due in part, to the reactive oxygen species quenching ability of these carotenoids. Lutein is more stable to decomposition by pro-oxidants than are other carotenoids such as beta-carotene and lycopene. Lutein is abundant in the region surrounding the fovea, and lutein is the predominant pigment at the outermost periphery of the macula. Zeaxanthin, which is fully conjugated (lutein is not), may offer somewhat better protection than lutein against phototoxic damage caused by blue and near-ultraviolet light radiation. Lutein is one of only two carotenoids that have been identified in the human lens, may be protective against age-related increases in lens density and cataract formation. Again, the possible protection afforded by lutein may be accounted for, in part, by its reactive oxygen species scavenging abilities. Carotenoids also provide protection from cancer. One of the mechanisms of this is by increasing the expression of the protein connexin-43, thereby stimulating gap junctional communication and preventing unrestrained cell proliferation.

Pharmacodynamics

Lutein was found to be present in a concentrated area of the macula, a small area of the retina responsible for central vision. The hypothesis for the natural concentration is that lutein helps protect from oxidative stress and high-energy light. Several studies show that an increase in macula pigmentation decreases the risk for eye diseases such as Age-related Macular Degeneration (AMD).

Mechanism of action

Tocopherol acts as a radical scavenger. It mainly acts as an antioxidant for lipid bilayers. Tocopherol's functions depend on the H-atom donating ability, location, and movement within the membrane, as well as the efficiency in the radical recycling by some cytosolic reductants such as ascorbate. Tocopherol actions are related to the trap of radicals, and it has been shown that even in the absence of substituents in the ortho-positions, tocopherol can trap more than two radicals. The type of radicals available for tocopherol are alkyl and peroxy.

Pharmacodynamics

The antioxidant effects of tocopherol can be translated into different changes at the pharmacodynamic level. In vitro studies have shown that this antioxidant activity can produce modification in protein kinase C (PKC) which will later be translated into an inhibition of cell death. Some other derivate effects are the anti-inflammatory properties of tocopherol which can be related to the modulation of cytokines or prostaglandins, prostanoids and thromboxanes.