MELASTINE

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

• Hyperpigmentation
• Melasma
• Age spots
• Sun damage
• Post-inflammatory hyperpigmentation

Dosage

Children: Refer to the BNF for Children for appropriate dosing information in pediatric patients.

Adults: Refer to the BNF for specific dosing recommendations, as dosages may vary based on formulation and clinical context.

Mechanism of action

Arbutin acts as a competitive inhibitor of the tyrosinase enzyme by binding to the L-tyrosine site, thereby suppressing melanogenesis. This inhibition reduces the conversion of L-tyrosine to melanin, leading to decreased pigmentation in the skin. Additionally, arbutin may downregulate tyrosinase expression, although studies show mixed results regarding this effect.

Pharmacodynamics

At non-toxic concentrations, arbutin effectively inhibits tyrosinase activity in human keratinocytes, resulting in reduced melanin synthesis. In cultured melanoma cells, arbutin demonstrated a concentration-dependent inhibition of melanin production without adversely affecting cell growth at lower concentrations. It also inhibits the stimulation of melanogenesis by α-MSH and can counteract oxidative stress in skin tissues.

Pharmacokinetics

The pharmacokinetics of arbutin, including absorption, distribution, metabolism, and excretion, are not well-characterized in the literature. However, it is known that arbutin is metabolized to hydroquinone in the body, which may contribute to its depigmenting effects. Further studies are warranted to clarify its pharmacokinetic profile.

Pregnancy

There are no well-controlled studies of arbutin in pregnant women. Caution is advised, and it should be used only if clearly needed.

Breast-feeding

It is not known whether arbutin is excreted in human milk. Caution should be exercised when administering to nursing mothers.

Storage

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

Formulations

• Topical creams
• Lotions
• Serums

Indications

• Scurvy prevention and treatment
• Antioxidant therapy
• Enhancement of iron absorption
• Support for immune function
• Skin health and collagen synthesis

Dosage

Children: Refer to the BNF for Children for specific dosing recommendations tailored to pediatric patients.

Adults: Refer to relevant clinical guidelines or BNF for specific dosing recommendations based on condition and individual patient factors.

Mechanism of action

Ascorbyl acts as a cofactor for the enzyme prolyl hydroxylase, which is necessary for collagen synthesis. It also serves as an antioxidant by scavenging reactive oxygen species (ROS) and regenerating other antioxidants, such as vitamin E. This property helps to protect cells from oxidative stress and contributes to the maintenance of a healthy immune system.

Pharmacodynamics

Ascorbyl exhibits its pharmacological effects primarily through its antioxidant activity and its role in collagen biosynthesis. The vitamin's capacity to donate electrons allows it to neutralize free radicals, thereby preventing damage to cellular components. Additionally, ascorbyl enhances the absorption of non-heme iron from plant-based sources, aiding in the prevention of iron deficiency anemia. It also plays a role in the modulation of immune responses, supporting the body's defense mechanisms.

Pharmacokinetics

Ascorbyl is rapidly absorbed from the gastrointestinal tract, with peak plasma concentrations occurring approximately 2 hours after oral administration. It is distributed throughout the body, with higher concentrations found in adrenal glands, pituitary glands, and leukocytes. Ascorbyl is primarily excreted via the kidneys, and its plasma half-life is approximately 16 to 20 days at normal dietary intake levels. The elimination of ascorbic acid occurs through renal excretion, with significant amounts excreted when plasma concentrations exceed the renal threshold.

Adverse effects

• Gastrointestinal disturbances
• Diarrhea
• Nausea
• Abdominal cramps
• Kidney stones (in high doses)

Interactions

• May enhance the effects of iron supplements
• May reduce the efficacy of some chemotherapeutic agents
• May interfere with certain laboratory tests (e.g., glucose tests)

Precautions

• Use with caution in patients with a history of kidney stones
• Monitor for gastrointestinal side effects in sensitive individuals
• Consider potential interactions with other medications

Pregnancy

Ascorbic acid is generally regarded as safe during pregnancy when used in recommended doses. Excessive doses should be avoided.

Breast-feeding

Ascorbic acid is excreted in breast milk. It is considered safe during breastfeeding when used at recommended doses.

Storage

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

Formulations

• Oral tablets
• Effervescent tablets
• Powder for solution
• Injection

Indications

• Used as a surfactant in drug formulations
• Enhancing the bioavailability of poorly soluble drugs
• Potential use in targeted drug delivery systems

Dosage

Children: Refer to specific product guidelines as dosing will vary based on formulation and intended use.

Adults: Refer to specific product guidelines as dosing will vary based on formulation and intended use.

Mechanism of action

Dipalmitate acts primarily by forming lipid bilayers that mimic biological membranes, facilitating drug incorporation and release. It enhances the solubility of hydrophobic drugs by creating a hydrophilic environment, aiding in their absorption. Additionally, it may promote the fusion of liposomes with cell membranes, thereby enhancing cellular uptake.

Pharmacodynamics

The pharmacodynamic properties of dipalmitate are largely attributed to its ability to interact with biological membranes. It influences membrane fluidity and permeability, which can affect the transport and absorption of co-administered drugs. This surfactant action can lead to improved therapeutic efficacy of various formulations by enhancing drug solubility and stability.

Pharmacokinetics

Dipalmitate is generally not absorbed systemically when used in pharmaceutical formulations due to its large molecular weight and lipophilic nature. When administered orally or topically, it primarily acts locally at the site of application. The metabolism of dipalmitate is not well characterized, but it is likely to be broken down into its constituent fatty acids and glycerol by lipolytic enzymes, with the fatty acids being utilized for energy or re-esterified for storage.

Pregnancy

Dipalmitate is generally considered safe during pregnancy, but it should be used only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Dipalmitate is excreted in breast milk; caution should be exercised when administering to nursing mothers.

Storage

Store at room temperature, away from moisture and heat. Protect from light.

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.

Indications

• Hyperpigmentation
• Melasma
• Age spots
• Other skin discolorations

Dosage

Children: The safety and efficacy of kojic acid in pediatric populations have not been well established. It is advisable to consult with a healthcare professional before using this product on children.

Adults: Kojic acid is typically used in concentrations ranging from 1% to 4% in topical formulations. Directions for use depend on the specific product and should be followed as indicated on the product label.

Mechanism of action

Kojic acid primarily acts as a tyrosinase inhibitor, reducing melanin production by inhibiting the conversion of tyrosine to melanin. This mechanism is pivotal in addressing various pigmentation disorders, making kojic acid an effective agent in skin lightening and treatment of hyperpigmentation.

Pharmacodynamics

Kojic acid exhibits skin depigmenting effects through its inhibition of the enzyme tyrosinase, leading to decreased melanin synthesis. This property is beneficial in treating skin conditions characterized by excessive pigmentation. In addition to its depigmenting effects, kojic acid has been noted to possess antioxidant properties, which can contribute to skin health by combating oxidative stress.

Pharmacokinetics

Kojic acid is readily absorbed through the skin when applied topically. Its systemic absorption is typically low, which minimizes the risk of systemic side effects. The compound is metabolized in the liver, and its metabolites are excreted primarily through urine. The half-life and specific pharmacokinetic parameters may vary based on formulation and individual skin characteristics.

Adverse effects

• Skin irritation
• Allergic contact dermatitis
• Hypopigmentation
• Photosensitivity

Precautions

• Not recommended for use in individuals with a known hypersensitivity to kojic acid or its derivatives.
• Should be used with caution in patients with sensitive skin.

Pregnancy

Kojic acid should be used with caution during pregnancy. There is limited data on its safety.

Breast-feeding

Kojic acid is not known to be excreted in breast milk, but caution is advised when used by nursing mothers.

Storage

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

Formulations

• Topical cream
• Gel
• Serum
• Soap

Indications

• Type 2 diabetes management
• Hyperlipidemia
• Hypertension
• Respiratory disorders
• Antioxidant support

Dosage

Children: Pediatric dosing should be determined by a healthcare provider based on individual needs and product formulations. Refer

Adults: Dosage varies based on the form and concentration of mulberry product. General recommendations for powdered mulberry leaf range from 1 to 3 grams per day. For extracts, follow manufacturer instructions or consult a healthcare provider.

Mechanism of action

The active compounds in mulberry, including flavonoids, phenolic acids, and alkaloids, exert their effects through various mechanisms. These compounds can inhibit α-glucosidase, an enzyme responsible for breaking down carbohydrates into glucose, thereby reducing postprandial blood glucose levels. Additionally, mulberry extracts have shown potential in modulating insulin sensitivity and exerting antioxidant effects, which may contribute to their therapeutic benefits in metabolic disorders.

Pharmacodynamics

The pharmacodynamic effects of mulberry are primarily related to its ability to influence glucose metabolism, lipid profiles, and inflammation. Mulberry extracts have demonstrated the ability to lower blood sugar levels and improve insulin sensitivity, which is beneficial for individuals with type 2 diabetes. Antioxidant properties are attributed to the presence of flavonoids, which can scavenge free radicals and reduce oxidative stress, potentially offering protective effects against chronic diseases.

Pharmacokinetics

The pharmacokinetics of mulberry are not as well characterized as those of pharmaceutical agents. However, it is believed that the bioactive compounds are absorbed through the gastrointestinal tract. Factors such as the form of mulberry (e.g., extract, powder) and the presence of other food substances can influence the absorption and bioavailability of its active constituents. Metabolism occurs primarily in the liver, and elimination of these compounds is likely through renal pathways.

Adverse effects

• Gastrointestinal upset
• Allergic reactions
• Hypoglycemia

Interactions

• Potential interactions with antidiabetic medications
• May affect blood glucose levels when taken with other hypoglycemic agents

Precautions

• Use with caution in patients with diabetes
• Monitor blood sugar levels regularly

Pregnancy

There is insufficient reliable information regarding the safety of mulberry during pregnancy. Consult a healthcare provider.

Breast-feeding

Limited information is available on the excretion of mulberry in breast milk. Consult a healthcare provider before use.

Storage

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

Formulations

• Dried fruit
• Powder
• Extract
• Tea

Indications

• Vitamin E deficiency
• Prevention of oxidative stress-related conditions
• Support for immune function
• Potential adjunctive therapy in chronic diseases such as coronary heart disease and cancer

Dosage

Adults: Refer to

Mechanism of action

The precise mechanisms of vitamin E's actions are not fully understood; however, it is known to act as an antioxidant by preventing free radical reactions with cell membranes. One key mechanism involves the termination of lipid peroxidation, where vitamin E interacts with unstable lipid radicals to produce stable lipids and a relatively stable vitamin E radical. This radical can be regenerated back to its active form through reactions with ascorbate or glutathione. Additionally, vitamin E may modulate inflammatory responses and is linked to cancer prevention through its effects on NF-kappaB signaling pathways.

Pharmacodynamics

Vitamin E functions primarily as an antioxidant, protecting cells against oxidative stress and inflammatory processes. It helps to mitigate the damaging effects of reactive oxygen species (ROS) and is vital in maintaining the integrity of cell membranes. Vitamin E deficiency can lead to various health issues, including impaired immune function and increased susceptibility to chronic diseases such as coronary heart disease and certain cancers. It also plays a role in safeguarding other fat-soluble vitamins from oxidative degradation.

Pharmacokinetics

Tocopheryl is absorbed through the intestinal tract and is typically transported in the bloodstream by lipoproteins. The bioavailability of vitamin E can be influenced by dietary fat intake, as it is fat-soluble. Once absorbed, tocopheryl is stored in the liver and adipose tissues. The metabolism of vitamin E involves conversion to various metabolites, which can be excreted in urine and bile. The half-life of alpha-tocopherol in the body can vary, but it is generally several hours to days, depending on individual factors and dietary intake.

Adverse effects

• Nausea
• Diarrhea
• Abdominal cramps
• Fatigue
• Headache

Interactions

• May enhance the effects of anticoagulants, increasing the risk of bleeding
• May interact with statins, potentially increasing risk of muscle disorders
• May reduce the effectiveness of certain chemotherapy agents

Precautions

• Use with caution in individuals with a history of bleeding disorders
• Monitor prothrombin time in patients on anticoagulants
• Consult healthcare provider before use in pregnant or breastfeeding women

Pregnancy

Vitamin E is generally considered safe during pregnancy when used in recommended amounts, but high doses should be avoided as they may pose risks.

Breast-feeding

Vitamin E is excreted in breast milk; consult a healthcare provider before supplementation while breastfeeding.

Storage

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

Formulations

• Capsules
• Soft gels
• Liquid formulations
• Tablets

Indications

• Heavy menstrual bleeding (menorrhagia)
• Surgical procedures to reduce blood loss
• Trauma-related bleeding
• Hereditary angioedema
• Dental procedures in patients with bleeding disorders

Dosage

Children: Refer to the BNF for Children for specific dosing guidelines based on age, weight, and indication.

Adults: Refer to the BNF for specific dosing guidelines based on indication and patient condition.

Mechanism of action

Tranexamic acid competitively inhibits the lysine binding sites on plasminogen, preventing its conversion to plasmin. This inhibition decreases fibrinolysis, leading to increased clot stability and reduced bleeding.

Pharmacodynamics

The primary pharmacodynamic effect of tranexamic acid is its ability to reduce bleeding by stabilizing fibrin clots. The drug exhibits a dose-dependent effect on clotting, with higher doses leading to a more pronounced antifibrinolytic effect. Tranexamic acid does not significantly affect platelet function or coagulation factors.

Pharmacokinetics

Tranexamic acid is rapidly absorbed after oral administration, with peak plasma concentrations occurring within 1 to 3 hours. It has a bioavailability of approximately 30% to 50%. The drug is primarily excreted unchanged in the urine, with a half-life of approximately 2 hours. It does not undergo significant metabolism in the liver, which is beneficial in patients with hepatic impairment.

Contra-indications

• Active venous thromboembolism
• History of thromboembolic disorders
• Severe renal impairment
• Hypersensitivity to tranexamic acid or any excipients

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Abdominal pain
• Dizziness
• Headache
• Visual disturbances
• Thrombosis
• Hypotension
• Allergic reactions

Interactions

• Anticoagulants (increased risk of thrombosis)
• Hormonal contraceptives (increased risk of thrombosis)
• Fibrinolytics (increased risk of bleeding)

Precautions

• Monitor for signs of thrombosis during treatment
• Use with caution in patients with a history of seizures
• Caution in patients with renal impairment
• Assess the risk of bleeding before use

Pregnancy

Tranexamic acid should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Tranexamic acid is excreted in breast milk; caution should be exercised when administered to nursing mothers.

Storage

Store at room temperature, away from moisture and direct sunlight. Keep out of reach of children.

Formulations

• Tablets
• Injection solution

Mechanism of action

Arbutin is a hydroquinone glycoside, however the hydroquinone moiety is not solely responsible for the de-pigmentating actions of arbutin. It acts as a competitive inhibitor of tyrosinase enzyme by acting on the L-tyrosine binding site to suppress melanogenesis and mediate its de-pigmenting actions on human skin. Tyrosinase is an enzyme involved in the regulation of rate-limiting steps during the synthesis of melanin; it regulates the conversion of L-tyrosine into L-dopa, and subsequent conversion of L-dopa to L-dopaquinone. Via inhibition of tyrosinase activity in a concentration-dependent manner, arbutin attenuates the production of melanin in melanocytes. While most studies suggest that arbutin has negligible effect on the tyrosinase mRNA expression, a study assessing the effect of arbutin on melanocyte differentiation inducement system using ES cells propose that arbutin may also downregulate the expression of tyrosinase in addition to its inhibitory action on the enzyme. The contradictory findings across studies may be due to previous studies using terminally-differentiated melanocytes and melanoma cells. ...This study ... presents evidence that cotreatment of aloesin and arbutin inhibits tyrosinase activity in a synergistic manner by acting through a different action mechanism. Aloesin or arbutin similarly inhibited enzyme activity of human- and mushroom-tyrosinases with an IC50 value of 0.1 or 0.04 mM, respectively. Lineweaver-Burk plots of the enzyme kinetics data showed that aloesin inhibited tyrosinase activity noncompetitively with a Ki value of 5.3 mM, whereas arbutin did it competitively (Maeda, 1996). We then examined whether cotreatment of these agents inhibits the tyrosinase activity in a synergistic manner. The results showed that 0.01 mM aloesin in the presence of 0.03 mM arbutin inhibited activity of mushroom by 80% of the control value and the reverse was also true. The inhibitory effects were calculated to be synergistic according to the Burgi method. Taken together, we suggest that aloesin along with arbutin inhibits in synergy melanin production by combined mechanisms of noncompetitive and competitive inhibitions of tyrosinase activity.

Pharmacodynamics

At non-toxic concentrations, arbutin inhibited the activity of tyrosinase in cultured human keratinocytes, while having minimal effect on the expression of tyrosinase mRNA or the synthesis of the enzyme. α-Arbutin produced a concentration-dependent inhibition of melanin synthesis of human melanoma cells, HMV-II. No inhibitory effect on HMV-II cell growth was seen at concentrations lower than 1.0 mM. At concentrations of 0.5 mM of arbutin, tyrosinase activity was reduced to 60% of that in non-treated cells. The addition of arbutin blocked and inhibited α-MSH-stimulated melanogenesis in B16 melanoma cells, brownish guinea pig, and human skin tissue. In a pilot study of healthy male adults exposed to UV B irradiation, topical administration of arbutin inhibited UV-induced nuclear factor-kappaB activation in human keratinocytes. In mouse skin, arbutin counteracted oxidative stress induced by 12-O-tetradecanoylphorbol-13-acetate.

Mechanism of action

The mechanism of action for most of vitamin E's effects are still unknown. Vitamin E is an antioxidant, preventing free radical reactions with cell membranes. Though in some cases vitamin E has been shown to have pro-oxidant activity. One mechanism of vitamin E's antioxidant effect is in the termination of lipid peroxidation. Vitamin E reacts with unstable lipid radicals, producing stable lipids and a relatively stable vitamin E radical. The vitamin E radical is then reduced back to stable vitamin E by reaction with ascorbate or glutathione. Cancer development and progression are closely associated with inflammation. NF-kappaB (nuclear factor kappaB) provides a mechanistic link between inflammation and cancer, and is a major factor controlling the ability of malignant cells to resist tumor surveillance mechanisms. NF-kappaB might also regulate tumor angiogenesis and invasiveness and the signalling pathways that mediate its activation provide attractive targets for new chemopreventive and chemotherapeutic approaches. ROS (reactive oxygen species) initiate inflammation by up-regulation of pro-inflammatory cytokines and therefore antioxidants provide a major defence against inflammation. alpha-Tocopherol is a lipid-soluble antioxidant. In addition to decreasing lipid peroxidation, alpha-tocopherol may exert intracellular effects. Hence, the aim of this study was to test the effect of alpha-tocopherol supplementation in cancer prevention via suppression of NF-kappaB-mediated pro-inflammatory cytokines. alpha-Tocopherol treatment significantly down-regulates expression, synthesis as well as secretion of pro-inflammatory cytokine IL-6 (interleukin-6) in cancerous mice. It also suppresses NF-kappaB binding to IL-6 promoter in liver leading to decreased secretion of IL-6 in serum. The regulation of the signalling pathway by alpha-tocopherol is found apart from its antioxidant capacity to reduce lipid peroxidation. Thus, the present study provides evidence for the hypothesis that besides the powerful free radical scavenging effects, alpha-tocopherol has genomic effects in down-regulation of pro-inflammatory cytokine and cancer prevention via the NF-kappaB-dependent pathway. Mitocans are drugs selectively killing cancer cells by destabilizing mitochondria and many induce apoptosis via generation of reactive oxygen species (ROS). However, the molecular events by which ROS production leads to apoptosis has not been clearly defined. In this study with the mitocan alpha-tocopheryl succinate (alpha-TOS) the role of the Bcl-2 family proteins in the mechanism of malignant cell apoptosis has been determined. Exposure of several different cancer cell lines to alpha-TOS increased expression of the Noxa protein, but none of the other proteins of the Bcl-2 family, an event that was independent of the cellular p53 status. alpha-TOS caused a profound conformational change in the pro-apoptotic protein, Bak, involving oligomerization in all cell types, and this also applied to the Bax protein, but only in non-small cell lung cancer cells. Immunoprecipitation studies indicated that alpha-TOS activates the two BH1-3 proteins, Bak or Bax, to form high molecular weight complexes in the mitochondria. RNAi knockdown revealed that Noxa and Bak are required for alpha-TOS-induced apoptosis, and the role of Bak was confirmed using Bak- and/or Bax-deficient cells. We conclude that the major events induced by alpha-TOS in cancer cells downstream of ROS production leading to mitochondrial apoptosis involve the Noxa-Bak axis. It is proposed that this represents a common mechanism for mitochondrial destabilization activated by a variety of mitocans that induce accumulation of ROS in the early phases of apoptosis. /alpha-Tocopheryl succinate/

Pharmacodynamics

Vitamin E is a collective term used to describe 8 separate fat soluble antioxidants, most commonly alpha-tocopherol. Vitamin E acts to protect cells against the effects of free radicals, which are potentially damaging by-products of the body's metabolism. Vitamin E deficiency is seen in persons with abetalipoproteinemia, premature, very low birth weight infants (birth weights less than 1500 grams, or 3½ pounds), cystic fibrosis, and cholestasis and severe liver disease. Preliminary research suggests vitamin E may help prevent or delay coronary heart disease and protect against the damaging effects of free radicals, which may contribute to the development of chronic diseases such as cancer. It also protects other fat-soluble vitamins (A and B group vitamins) from destruction by oxygen. Low levels of vitamin E have been linked to increased incidence of breast and colon cancer.