CELLGIVITY CAPSULES

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)

Dosage

Children: Paediatric dosing for blends is not commonly standardized and should be approached with caution. Consultation with a healthcare provider is recommended to determine appropriate dosing based on the specific blend and the child's health needs.

Adults: Dosage for adult blends varies widely depending on the specific formulation and purpose. It is important to refer to the specific product label or consult a healthcare professional for guidance.

Mechanism of action

The mechanism of action for a blend depends on its individual components. For example, if the blend contains herbal extracts, each herb may have its own active compounds that interact with various biochemical pathways in the body, such as antioxidant activity, anti-inflammatory effects, or modulation of neurotransmitter levels. These mechanisms can vary significantly based on the specific herbs or substances included in the blend.

Pharmacodynamics

Pharmacodynamics of a blend involves understanding how the individual components affect the body. This can include synergistic effects where the combined action of substances leads to enhanced therapeutic effects, or antagonistic effects where one substance may reduce the efficacy of another. The overall pharmacodynamic profile will depend on the blend's composition and the dose of each ingredient.

Pharmacokinetics

Pharmacokinetics of a blend varies based on the components used. Factors such as absorption, distribution, metabolism, and excretion can change according to the specific substances involved. For instance, some herbal constituents may be rapidly absorbed, while others might have delayed onset of action due to slow metabolism or elimination processes. The presence of multiple ingredients may also influence the pharmacokinetics of each other through various interactions.

Pregnancy

Consult a healthcare provider before use. The effects on fetal development are not well-studied, and potential risks should be assessed based on the specific formulation and individual health circumstances.

Breast-feeding

Consult a healthcare provider before use. Safety during breastfeeding is not well-established, and potential risks to the infant should be considered.

Storage

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

Dosage

Children: For paediatric dosing recommendations, consult relevant pediatric prescribing guidelines or the BNF for Children.

Adults: For specific dosing information, refer to the appropriate clinical guidelines or product literature, as proprietary drugs can vary widely in their indications and dosing recommendations.

Mechanism of action

The mechanism of action of proprietary drugs varies widely depending on the active ingredients they contain. Generally, they work by interacting with specific biological pathways or targets in the body. These may include receptor modulation, enzyme inhibition, or alteration of cellular signaling pathways, leading to a desired therapeutic effect. For example, some proprietary drugs may act as agonists or antagonists at particular receptors, influencing physiological responses.

Pharmacodynamics

Pharmacodynamics of proprietary drugs involves understanding how the drug affects the body. This includes the relationship between the drug concentration and its therapeutic effect, as well as the time course of its action. Proprietary formulations may exhibit dose-dependent effects, where increasing doses lead to enhanced therapeutic outcomes up to a certain threshold, after which adverse effects may occur. Factors such as receptor affinity, intrinsic activity, and the drug's therapeutic window are critical in determining its pharmacodynamics.

Pharmacokinetics

Pharmacokinetics describes how the body absorbs, distributes, metabolizes, and excretes proprietary drugs. This includes the drug's bioavailability, volume of distribution, half-life, and clearance rates. Proprietary formulations may utilize specific delivery systems to enhance absorption or modify the release profile, affecting how quickly the drug reaches systemic circulation and its duration of action. Metabolism typically occurs in the liver, where cytochrome P450 enzymes may play a significant role, and excretion can occur via renal or biliary pathways.

Pregnancy

Consult relevant guidelines; data on safety in pregnancy may vary.

Breast-feeding

Consult relevant guidelines; data on safety during breastfeeding may vary.

Storage

Store in a cool, dry place away from light.

Indications

• Supporting glutathione synthesis
• Potential use in conditions associated with oxidative stress
• Investigational roles in metabolic enhancement

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines.

Mechanism of action

Riboceine is believed to facilitate the transport of cysteine into cells, where it can be utilized for the synthesis of glutathione. This mechanism enhances the availability of cysteine, thus promoting the endogenous production of glutathione, which plays a critical role in detoxification and antioxidant defense mechanisms within the body.

Pharmacodynamics

Riboceine's pharmacodynamic properties include its ability to elevate intracellular levels of glutathione, thereby improving cellular resilience against oxidative damage. Increased glutathione levels can enhance detoxification processes, reduce oxidative stress, and may have a protective effect on various cellular functions.

Pharmacokinetics

The pharmacokinetics of riboceine, including its absorption, distribution, metabolism, and excretion, are not extensively documented. However, as a precursor to cysteine, it is likely that riboceine is absorbed through the gastrointestinal tract and enters systemic circulation, where it is utilized by cells for glutathione synthesis. Further studies are needed to clarify its pharmacokinetic profile.

Pregnancy

There is no data available on the safety of riboceine during pregnancy. Caution is advised.

Breast-feeding

There is no information available regarding the excretion of riboceine in human milk. Caution is advised.

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.