Berzol 5%

Indications

• Dry eye syndrome
• Ocular surface discomfort
• Environmental irritation to the eyes
• Post-surgical ocular dryness

Dosage

Children: Refer to specific product guidelines for paediatric dosing, as it may vary based on formulation and severity of symptoms.

Adults: Refer to specific product guidelines for adult dosing, as it may vary based on formulation and severity of symptoms.

Mechanism of action

Acrypol works by forming a viscoelastic gel on the ocular surface, which mimics natural tears. This gel formation helps to retain moisture and provide lubrication, alleviating symptoms of dryness and irritation. The polymer chains in Acrypol interact with the tear film and the corneal epithelium, promoting hydration and providing a protective barrier against environmental irritants.

Pharmacodynamics

The primary pharmacodynamic action of Acrypol is its ability to enhance tear film stability and increase ocular surface hydration. By improving lubrication, it helps reduce friction during blinking, thereby alleviating discomfort and preventing damage to the corneal epithelium. The viscosity of the formulation is crucial in ensuring prolonged contact time with the eye, which contributes to its therapeutic effect.

Pharmacokinetics

Acrypol is applied topically to the eyes, where it acts locally without significant systemic absorption. The polymeric nature of the formulation allows for sustained release and retention on the ocular surface. The clearance from the eye may vary depending on factors such as blinking rate and tear production, but generally, the formulation is designed for prolonged action.

Pregnancy

Safety during pregnancy has not been established. Use only if the benefits outweigh the risks.

Breast-feeding

Use with caution, as it is not known whether acrypol is excreted in human milk.

Storage

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

Indications

• Acne vulgaris
• Comedonal acne
• Inflammatory acne

Dosage

Children: Refer to the BNF for Children for specific dosing recommendations, as pediatric dosing may vary based on age and severity of condition.

Adults: Apply a thin layer to the affected area once or twice daily, gradually increasing frequency as tolerated. Start with once daily application and may increase to twice daily after a week if skin irritation is manageable.

Mechanism of action

The peroxide bond of benzoyl peroxide is cleaved to form two benzoyloxy radicals. These radicals nonspecifically interact with bacterial proteins, disrupting their function and survival. This leads to a reduction in keratin and sebum accumulation around hair follicles. Additionally, benzoyl peroxide enhances the turnover rate of epithelial cells, facilitating skin peeling and helping to break down comedones.

Pharmacodynamics

Benzoyl peroxide acts as a topical agent that generates free radicals to effectively break down comedones and promote epithelial cell turnover. Its action is short-lived, as the active free radical metabolites quickly react to form inactive compounds. The therapeutic index is wide, with rare occurrences of overdose, although skin irritation, dryness, and increased susceptibility to sunburn are common side effects.

Pharmacokinetics

Benzoyl peroxide is applied topically, leading to localized effects with minimal systemic absorption. Its rapid conversion into inactive metabolites limits its duration of action. The compound is metabolized in the skin, and its peak effects are typically observed shortly after application. Due to its formulation and route of administration, the pharmacokinetic profile is characterized by a localized action with reduced risk of systemic side effects.

Adverse effects

• Skin irritation
• Dryness
• Sunburn
• Peeling of skin

Precautions

• Avoid contact with eyes and mucous membranes
• Use with caution in patients with sensitive skin

Pregnancy

Benzoyl peroxide is generally considered safe for use during pregnancy, but it is advisable to consult a healthcare professional before use.

Breast-feeding

Benzoyl peroxide is excreted in breast milk in small amounts. Consult a healthcare professional before use while breastfeeding.

Storage

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

Formulations

• Topical gel
• Topical cream
• Topical lotion

Indications

• Alcohol use disorder
• Acute alcohol intoxication
• Antiseptic for skin disinfection

Mechanism of action

Ethanol affects the brain’s neurons in several ways. It alters their membranes, ion channels, enzymes, and receptors. Ethanol binds directly to the receptors for acetylcholine, serotonin, GABA, and NMDA receptors for glutamate. The sedative effects are mediated through binding to GABA receptors and glycine receptors, while also inhibiting NMDA receptor functioning. As an anti-infective, ethanol acts as an osmolyte, disrupting the osmotic balance across cell membranes. The acute effects result from competitive inhibition of glycine binding to NMDA receptors, leading to disrupted glutamatergic neurotransmission.

Pharmacodynamics

Ethanol produces cellular injury through dehydration and precipitation of cytoplasm, contributing to its bactericidal and antifungal actions. It can lead to neuritis and nerve degeneration when injected near nerve tissues. Up to 98% of ethanol in the body is oxidized, primarily by the hepatic enzyme alcohol dehydrogenase. Its modulation of neurotransmitter receptors, particularly GABA and NMDA, leads to its sedative properties and potential for developing tolerance with chronic use.

Pharmacokinetics

Ethanol is readily absorbed from the gastrointestinal tract and distributed throughout the body. It has a volume of distribution of approximately 0.5 to 0.6 L/kg. Ethanol is metabolized predominantly in the liver by alcohol dehydrogenase to acetaldehyde, which is further oxidized to acetic acid by aldehyde dehydrogenase. The elimination half-life of ethanol varies but is generally around 4 to 5 hours. Factors such as age, sex, body weight, and genetic variability can influence ethanol metabolism.

Contra-indications

• Hypersensitivity to ethanol
• Acute alcohol intoxication
• Severe liver disease
• Pregnancy (in non-medicinal use)
• Severe pancreatitis
• Severe head injury or intracranial bleeding

Adverse effects

• Dizziness
• Nausea
• Vomiting
• Headache
• Sedation
• Cognitive impairment
• Respiratory depression
• Hypotension
• Gastrointestinal bleeding
• Alcohol withdrawal syndrome

Interactions

• CNS depressants (e.g., benzodiazepines, opioids) may enhance sedative effects
• Disulfiram may cause unpleasant reactions when taken with ethanol
• Acetaminophen may increase hepatic toxicity when used with ethanol
• Warfarin may have altered effects when used with ethanol

Precautions

• Caution in patients with a history of alcohol abuse
• Use with caution in patients with hepatic impairment
• Monitor for signs of respiratory depression
• Consider potential for addiction and withdrawal symptoms
• Use in moderation in older adults due to increased sensitivity

Pregnancy

Ethanol should be avoided during pregnancy due to the risk of fetal alcohol spectrum disorders.

Breast-feeding

Ethanol can pass into breast milk; breastfeeding should be avoided for a minimum of 2 hours after consumption.

Storage

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

Formulations

• Oral solutions
• Topical antiseptics
• Intravenous formulations
• Medicinal tinctures

Dosage

Children: Refer to the BNF for Children for appropriate dosing information in paediatric cases, especially in instances of overdose.

Adults: Refer to the BNF for specific dosing information based on clinical circumstances, particularly in cases of overdose.

Mechanism of action

Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is subsequently converted to glycolic, glyoxylic, and oxalic acids. These metabolites contribute to anion gap metabolic acidosis and are responsible for tissue injury through the formation of insoluble calcium oxalate crystals.

Pharmacodynamics

The toxicity of ethylene glycol arises from its metabolites, particularly glycolic and oxalic acids. These compounds induce metabolic acidosis, lead to renal failure through calcium oxalate crystal deposition in the kidneys, and can cause neurological impairment. The anion gap increases due to the accumulation of these acids, leading to complications such as cardiovascular instability and potential multi-organ failure.

Pharmacokinetics

Ethylene glycol is rapidly absorbed after oral ingestion. It undergoes first-pass metabolism primarily in the liver, where it is converted into its toxic metabolites. The elimination half-life of ethylene glycol varies but is generally prolonged in cases of renal impairment. Renal excretion of metabolites contributes to the duration of toxicity, necessitating prompt medical intervention in cases of overdose.

Adverse effects

• Metabolic acidosis
• Renal failure
• CNS depression
• Hypocalcemia
• Cardiovascular collapse
• Pulmonary edema

Precautions

• Use with caution in patients with renal impairment
• Monitor for signs of metabolic acidosis
• Evaluate electrolyte levels, particularly calcium

Pregnancy

There is limited data on the safety of ethylene glycol in pregnancy. It should only be used if clearly needed.

Breast-feeding

It is unknown if ethylene glycol is excreted in human milk. Caution is advised.

Storage

Store in a tightly closed container at room temperature, away from heat and moisture.

Formulations

• Liquid

Indications

• Solvent in pharmaceutical formulations
• Moisturizer and humectant in topical applications
• Potential use in the management of drug solubility issues

Dosage

Children: Refer to specific formulations and clinical guidelines, as dosing varies widely based on the application and formulation.

Adults: Refer to specific formulations and clinical guidelines, as dosing varies widely based on the application and formulation.

Mechanism of action

Glycols, particularly propylene glycol, act as humectants, which help to retain moisture in formulations. They can also enhance the solubility of drugs, aiding in their absorption when used as excipients. Propylene glycol is metabolized in the liver to lactate and subsequently to glucose, providing a source of energy when utilized in metabolic pathways.

Pharmacodynamics

The pharmacodynamics of glycols involve their ability to modulate the viscosity of solutions and enhance the solubility of other compounds. Propylene glycol can also facilitate the absorption of other drugs when used in formulations. It exhibits a low toxicity profile when used appropriately, but excessive systemic exposure can lead to metabolic acidosis and other adverse effects.

Pharmacokinetics

Glycols are rapidly absorbed when administered intravenously or orally. Propylene glycol is metabolized primarily in the liver, with a half-life varying based on the dose and individual metabolism. Renal excretion plays a role in the elimination of metabolites. Accumulation can occur in individuals with impaired liver or kidney function, necessitating careful monitoring of dosing in such populations.

Pregnancy

The safety of glycol in pregnancy is not well established. Consult healthcare professionals before use.

Breast-feeding

Glycol's effects during breastfeeding are not well characterized. Caution is advised.

Storage

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

Dosage

Children: Refer to specific guidelines for pediatric dosing; consult the BNF for Children for accurate dosage information.

Adults: Refer to specific guidelines for use; dosage may vary based on the context of use.

Mechanism of action

Hydroxide ions act primarily as bases, neutralizing acids to form water and salts. They participate in various biochemical pathways, including selenium metabolism and the degradation of reactive oxygen species. Hydroxide can influence enzyme activity and stability by altering the pH of the environment, thereby affecting metabolic reactions.

Pharmacodynamics

Hydroxide ions can impact biological processes by changing the local pH, which influences enzyme activity, ion transport, and the solubility of other compounds. Their ability to neutralize acids can help regulate physiological pH, contributing to homeostasis in living organisms.

Pharmacokinetics

As an inorganic ion, hydroxide does not undergo traditional pharmacokinetic processes like absorption, distribution, metabolism, or excretion. Instead, it is rapidly equilibrated in biological fluids and participates in acid-base reactions, having immediate effects on the local environment.

Pregnancy

There is limited information regarding the use of hydroxide during pregnancy. Consult a healthcare professional for advice.

Breast-feeding

Limited data is available on the excretion of hydroxide in breast milk. Consult a healthcare professional before use.

Storage

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

Indications

• Topical antiseptic for minor cuts and abrasions
• Wound cleansing
• Deodorizing agent

Dosage

Children: For paediatric use, hydrogen peroxide can be applied topically as a 3% solution. Consult the BNF for Children for detailed dosing guidance.

Adults: Hydrogen peroxide is typically applied topically as a 3% solution. It can be used to cleanse the affected area one to three times daily. For specific dosing, refer to the BNF.

Mechanism of action

The production of free hydroxyl radicals in the Fenton reaction is thought to be the basis of the biocidal actions of hydrogen peroxide. Free radicals lead to oxidative damage to proteins and membrane lipids in vivo. The release of nascent oxygen upon contact with catalase-containing tissues exerts antibacterial action, while effervescence mechanically loosens tissue debris and pus. Hydrogen peroxide is particularly effective on wounds, denuded areas, and mucous membranes.

Pharmacodynamics

Hydrogen peroxide exhibits antimicrobial properties against a wide range of microorganisms, including resistant forms such as bacterial spores and protozoal cysts. It acts as an oxidative biocide, generating free radicals that induce damage to DNA, proteins, and membrane lipids via oxidation. Its mechanical action of effervescence assists in the removal of tissue debris, which is a crucial aspect of its effectiveness in wound management.

Pharmacokinetics

Hydrogen peroxide's pharmacokinetics are not extensively detailed in the literature, but it is known to have poor tissue and wound penetration. The presence of reactive organic materials, such as pus and blood, diminishes its efficacy. The mechanical action of effervescence is significant in enhancing its antibacterial effects, particularly in contaminated wounds.

Adverse effects

• Skin irritation
• Burning sensation
• Allergic reactions

Precautions

• Avoid contact with eyes and mucous membranes
• Use with caution in patients with a history of hypersensitivity
• Do not apply to deep or puncture wounds

Pregnancy

Hydrogen peroxide should be used in pregnancy only if the potential benefit justifies the potential risk to the fetus. Consult a healthcare provider before use.

Breast-feeding

Caution is advised when using hydrogen peroxide while breastfeeding. Consult a healthcare provider for guidance.

Storage

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

Formulations

• Topical solution
• Ointment

Indications

• Constipation
• Bowel preparation prior to surgical procedures or diagnostic tests

Dosage

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

Adults: Refer to specific guidelines or BNF for detailed dosing information.

Mechanism of action

Polyethylene glycol works by osmotically retaining water in the intestinal lumen, which increases the water content of the stool. This enhances the passage of stool through the intestines and promotes bowel movements. The high molecular weight of polyethylene glycol prevents its absorption in the gastrointestinal tract, ensuring that it remains in the lumen to exert its effects.

Pharmacodynamics

The pharmacodynamic profile of polyethylene glycol involves its ability to increase stool water content, thereby reducing stool consistency and facilitating easier passage. It does not stimulate intestinal motility directly but rather relies on the osmotic effect to promote bowel evacuation. The onset of action typically occurs within 24 to 96 hours after ingestion.

Pharmacokinetics

Polyethylene glycol is not absorbed systemically, and its pharmacokinetics are characterized by its presence solely in the gastrointestinal tract. It is excreted unchanged in the stool. The volume of polyethylene glycol administered can influence the effectiveness and timing of its action, but its absorption is negligible, making systemic side effects rare.

Adverse effects

• Abdominal cramping
• Diarrhea
• Nausea
• Vomiting
• Bloating
• Flatulence

Precautions

• Use with caution in patients with gastrointestinal disorders or bowel obstruction.
• Ensure adequate hydration during use to prevent dehydration.

Pregnancy

Polyethylene glycol is generally considered safe during pregnancy, but should be used under medical supervision.

Breast-feeding

Polyethylene glycol is excreted in breast milk in very small amounts and is generally regarded as safe during breastfeeding.

Storage

Store at room temperature, away from moisture and heat.

Formulations

• Powder for oral solution
• Liquid formulation

Indications

• Plant growth regulation
• Agricultural applications as a growth inhibitor

Dosage

Children: Not applicable.

Adults: Refer to the relevant agricultural guidelines for specific applications.

Mechanism of action

In an in vitro study, propylene acts as a plant growth inhibitor by inhibiting the oxidation of indole-3-acetic acid by peroxidase in the presence of superoxide anion radicals. This inhibition is linked to the activation of an iron complex (compound III) shuttle, which enhances the reaction rate between superoxide and peroxidase, ultimately affecting plant growth processes. Propylene is a less effective inhibitor compared to ethylene.

Pharmacodynamics

The pharmacodynamic effects of propylene are primarily observed in its role as a growth inhibitor in plants. By modulating the oxidation of phytohormones like indole-3-acetic acid, propylene can influence various growth responses in plants, potentially affecting processes such as cell elongation and division.

Pharmacokinetics

Information on the pharmacokinetics of propylene in humans is not well-documented, as its primary uses are industrial and agricultural. Its metabolism may be influenced by environmental factors, and its effects are primarily studied in the context of plant biology rather than human pharmacology.

Dosage

Children: Refer to specific drug formulations and product labels as purified substances can vary widely in their use and dosing.

Adults: Refer to specific drug formulations and product labels as purified substances can vary widely in their use and dosing.

Mechanism of action

The mechanism of action for purified compounds varies widely depending on the specific substance. Generally, purified drugs exert their effects by interacting with specific biological targets, such as receptors, enzymes, or ion channels, leading to a desired therapeutic effect. This interaction can involve binding to receptors to activate or inhibit signaling pathways, modulating enzymatic activity, or altering physiological processes.

Pharmacodynamics

Pharmacodynamics describes the effects of a drug on the body and the relationship between drug concentration and effect. For purified drugs, this can involve dose-response relationships and the time course of their action. The purified form often enhances potency and reduces variability in response among patients, which can lead to more predictable therapeutic outcomes. The overall effect is determined by the drug's affinity for its target, the efficacy of the drug-receptor interaction, and the downstream signaling pathways activated as a result of this interaction.

Pharmacokinetics

Pharmacokinetics involves the absorption, distribution, metabolism, and excretion (ADME) of a drug. For purified substances, absorption can be more efficient due to the absence of impurities that may affect solubility or stability. Distribution may also be enhanced, leading to higher bioavailability. Metabolism can be influenced by the structure of the purified compound, as it may be metabolized more readily by liver enzymes. Excretion typically occurs through the kidneys or liver, depending on the molecular characteristics of the purified drug.

Pregnancy

Consult with a healthcare professional, as the safety of purified forms of medications during pregnancy may vary depending on the specific substance.

Breast-feeding

Consult with a healthcare professional, as the safety of purified forms of medications during breastfeeding may vary depending on the specific substance.

Storage

Store in a cool, dry place, away from light and moisture, and keep out of reach of children.

Indications

• Nutritional supplement for general health
• Support for immune system function
• Aid in recovery from illness
• Potential use in skin health and wound healing

Dosage

Children: There is no established specific dosage for children. Parents should consult a pediatrician or healthcare professional for appropriate advice based on the child's health needs and the product being used.

Adults: Typical dosages for adults vary widely depending on the formulation and intended use. Commonly, a daily dose of 1 to 3 grams of fresh royal jelly is suggested, but it is advisable to refer to specific product guidelines or consult a healthcare provider.

Mechanism of action

The exact mechanism of action of royal jelly is not fully understood. It is believed to exert its effects through various bioactive compounds, including proteins, lipids, and phenolic compounds, which may modulate immune responses, reduce oxidative stress, and influence hormonal activity. Additionally, royal jelly may enhance cellular metabolism and promote tissue regeneration.

Pharmacodynamics

Royal jelly exhibits a range of pharmacodynamic effects, including anti-inflammatory and antioxidant properties. It may enhance the immune response by stimulating various immune cells, including macrophages and lymphocytes. Its rich nutrient profile also contributes to its potential role in promoting cell growth and repair, impacting overall health and vitality.

Pharmacokinetics

The pharmacokinetics of royal jelly, including absorption, distribution, metabolism, and excretion, are not well-documented due to its complex composition. The bioactive components are likely absorbed in the gastrointestinal tract, but specific studies detailing their pharmacokinetic parameters are limited. Further research is required to elucidate these aspects fully.

Pregnancy

Safety during pregnancy has not been established. Consult a healthcare professional before use.

Breast-feeding

Consult a healthcare professional before use. Safety during breastfeeding is not well understood.

Storage

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

Mechanism of action

Acne vulgaris is caused by inflammation in the pilosebaceous gland. Acne is generally caused by increased excretion of sebum from pilosebaceous glands, endocrine factors such as androgenic hormones, keratin developing around follicles, bacterial growth, and inflammation. These factors contribute to the formation of comedones (whiteheads and blackheads). The peroxide bond of benzoyl peroxide is cleaved to form 2 benzoyloxy radicals. These radicals interact nonspecifically with bacterial proteins, interfering with their function, and survival of the bacteria. Over time, free radical interactions with bacterial proteins lead to decreased keratin and sebum around follicles. Benzoyl peroxide can also increase the turnover rate of epithelial cells, leading to skin peeling, and breaking down comedones.

Pharmacodynamics

Benzoyl peroxide is a topical treatment for acne that generates free radicals to break down comedones and increase the rate of epithelial cell turnover. It has a short duration of action as its active free radical metabolites quickly react to form inactive metabolites. The therapeutic index is wide, as overdoses are rare, however patients may still experience skin peeling. Patients should be counselled regarding increased risks of skin irritation, dryness, and sunburn.

Mechanism of action

Ethanol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate. The sedative effects of ethanol are mediated through binding to GABA receptors and glycine receptors (alpha 1 and alpha 2 subunits). It also inhibits NMDA receptor functioning. In its role as an anti-infective, ethanol acts as an osmolyte or dehydrating agent that disrupts the osmotic balance across cell membranes. ... Ethanol is known to affect a large number of membrane proteins that participate in signaling pathways such as neurotransmitter receptors, enzymes, and ion channels, and there is extensive evidence that ethanol interacts with a variety of neurotransmitters. The major actions of ethanol involve enhancing the inhibitory effects of gamma-aminobutyric acid (GABA) at GABAa receptors and blockade of the N-methyl-D-aspartate (NMDA) subtype of glutamate, an excitatory amine acid (EAA) receptor. Animal studies indicate that the acute effects of ethanol result from competitive inhibition of glycine binding to NMDA receptor and disruption of glutamatergic neurotransmission by inhibiting the response of the NMDA receptor. Persistent glycine antagonism and attenuation of glutamatergic neurotransmission by chronic ethanol exposure results in tolerance to ethanol by enhancing EAA neurotransmission and NMDA receptor upregulation. The latter appears to involve selective increases in NMDA R2B subunit concentrations and other molecular changes in specific brain loci. The abrupt withdrawal of ethanol thus produces a hyperexcitable state that leads to the ethanol withdrawal syndrome and excitotoxic neuronal death. GABA-mediated inhibition, which normally acts to limit excitation, is eliminated during ethanol withdrawal syndrome and further intensifies this excitation. In addition, NMDA receptors function to inhibit the release of dopamine in the nucleus accumbens and mesolimbic structures, which modulate the reinforcing action of addictive xenobiotics such as ethanol. By inhibiting NMDA receptor activity, ethanol could increase dopamine release from the nucleus accumbens and ventral tegmental area and could thus create dependence. Chronic ethanol administration also results in tolerance, dependence, and an ethanol withdrawal syndrome, mediated, in part, by desensitization and or downregulation of GABAa receptors. The development of alcoholic ketoacidosis (AKA) requires that a combination of physical and physiologic events occur. The normal response to starvation and depletion of hepatic glycogen stores is for amino acids to be converted to pyruvate. Pyruvate can serve as a substrate for gluconeogenesis, be converted to acetyl-CoA, which can enter the Krebs cycle or can be utilized in various biosynthetic pathways (eg, fatty acid, ketone bodies, cholesterol, and acetylcholine) ... Ethanol metabolism generates NADH, resulting in an excess of reducing potential. This high redox state favors the conversion of pyruvate to lactate, diverting pyruvate from being a substrate for gluconeogenesis. To compensate for the lack of normal metabolic substrates, the body mobilizes fat from adipose tissue and increased fatty acid metabolism as an alternative source of energy. This response is mediated by a decrease in insulin and an increased secretion of glucagon, catecholamines, growth hormone, and cortisol. Fatty acid metabolism results in the formation of acetyl-CoA and it combines with the excess acetate that is generated from ethanol metabolism to form acetoacetate. Most of the acetoacetate is reduced to beta-hydroxybutyrate due to the excess reducing potential or high redox state of the cell. Volume depletion interferes with the renal elimination of acetoacetate and beta-hydroxybutyrate, and contributes to the acidosis. An elevated lactate concentration may result from shunting from pyruvate or

Pharmacodynamics

Alcohol produces injury to cells by dehydration and precipitation of the cytoplasm or protoplasm. This accounts for its bacteriocidal and antifungal action. When alcohol is injected in close proximity to nerve tissues, it produces neuritis and nerve degeneration (neurolysis). Ninety to 98% of ethanol that enters the body is completely oxidized. Ethanol is also used as a cosolvent to dissolve many insoluble drugs and to serve as a mild sedative in some medicinal formulations. Ethanol also binds to GABA, glycine, NMDA receptors and modulates their effects. Ethanol is also metabolised by the hepatic enzyme alcohol dehydrogenase.

Mechanism of action

Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is then metabolized to glycolic, glyoxylic, and oxalic acids. These acids, along with excess lactic acid are responsible for the anion gap metabolic acidosis. Oxalic acid readily precipitates with calcium to form insoluble calcium oxalate crystals. Tissue injury is caused by widespread deposition of oxalate crystals and the toxic effects of glycolic and glyoxylic acids.

Mechanism of action

The production of free hydroxyl radicals in the Fenton reaction is thought to be the basis of biocidal actions of hydrogen peroxide. Free radicals eventually lead to oxidative damage proteins and membrane lipids _in vivo_. The oxidizing radical as the ferryl radical induces DNA oxidation. Hydrogen peroxide topical solution is a weak antibacterial agent, a wound cleanser, and a deodorant. The pharmacologic activity of the drug depends on the release of nascent oxygen which has a powerful oxidizing effect that destroys some microorganisms and chemically alters many organic substances. When hydrogen peroxide topical solution comes in contact with tissues that contain the enzyme catalase, the solution releases oxygen which exerts antibacterial action; the mechanical effect of effervescence loosens tissue debris and pus. The release of nascent oxygen and effervescence is more rapid on wounds, denuded areas, and mucous membranes than on unbroken skin. The presence of reactive organic material such as pus and blood diminishes the efficiency of hydrogen peroxide. The antibacterial activity of hydrogen peroxide is relatively weak and slow and the drug exhibits poor tissue and wound penetration. Hydrogen peroxide's mechanical effect of effervescence and resultant removal of tissue debris is probably a more effective means of reducing the bacterial content of wounds, denuded areas, and mucous membranes than actual antibacterial activity. The drug also appears to have a styptic effect when applied topically to minor wounds. Concentrated solutions of hydrogen peroxide have a bleaching effect on hair and may injure tissue. Increases in the levels of reactive oxygen species (ROS) are correlated with a decrease in calcineurin (CN) activity under oxidative or neuropathological conditions. However, the molecular mechanism underlying this ROS-mediated CN inactivation remains unclear. Here, we describe a mechanism for the inactivation of CN by hydrogen peroxide. The treatment of mouse primary cortical neuron cells with Abeta(1-42) peptide and hydrogen peroxide triggered the proteolytic cleavage of CN and decreased its enzymatic activity. In addition, hydrogen peroxide was found to cleave CN in different types of cells. Calcium influx was not involved in CN inactivation during hydrogen peroxide-mediated cleavage, but CN cleavage was partially blocked by chloroquine, indicating that an unidentified lysosomal protease is probably involved in its hydrogen peroxide-mediated cleavage. Treatment with hydrogen peroxide triggered CN cleavage at a specific sequence within its catalytic domain, and the cleaved form of CN had no enzymatic ability to dephosphorylate nuclear factor in activated T cells. Thus, our findings suggest a molecular mechanism by which hydrogen peroxide inactivates CN by proteolysis in ROS-related diseases. Matrix metalloproteinase-2 (MMP-2) is well known to proteolyse both extracellular and intracellular proteins. Reactive oxygen species activate MMP-2 at both transcriptional and post-translational levels, thus MMP-2 activation is considered an early event in oxidative stress injury. Although hydrogen peroxide is widely used to trigger oxidative stress-induced cell death, the type of cell death (apoptosis vs. necrosis) in cardiomyocytes is still controversial depending on the concentration used and the exposure time. We ... investigated the mode of cell death in neonatal rat cardiomyocytes induced by different concentrations (50-500 uM) of hydrogen peroxide at various time intervals after exposure and determined whether MMP-2 is implicated in hydrogen peroxide-induced cardiomyocyte death. Treating cardiomyocytes with hydrogen peroxide led to elevated MMP-2 level/activity with maximal effects seen at 200 uM. Hydrogen peroxide caused necrotic cell death by disrupting the plasmalemma as evidenced by the release of lactate dehydrogenase in a concentration- and time-dependent manner as well as the necrotic cleavage of PARP-1. The absence o

Pharmacodynamics

Hydrogen peroxide exhibits antimicrobial properties against most forms of microorganisms, including dormant forms with known high resistance profiles, such as bacterial spores and protozoal cysts. It acts as an oxidative biocide to generate free radical species to induce DNA, protein and membrane lipid damage via oxidation.

Mechanism of action

In an in vitro study of the mechanism of action of ethylene as a plant growth inhibitor, the effects of ethylene and some of its analogs, including propylene, on the oxidation of indole-3-acetic acid were examined. Ethylene and its analogs inhibited the oxidation of indole-3-acetic acid by peroxidase under conditions where the iron complex (compound III, an oxy-ferrous complex of peroxidase) shuttle was activated. Inhibition occurred only in the presence of the superoxide anion radical 02(-). Spectral and kinetic data indicated that ethylene and its analogs enhanced the rate of reaction of 02(-) with peroxidase; ie, the iron complex (compound III) shuttle, resulting in the formation of compound III. Propylene was a less effective inhibitor than ethylene.