Adalat LA 30mg tablets

Indications

• Dry eye conditions
• Tear deficiency
• Keratoconjunctivitis sicca

Dosage

Children: Apply as required, typically in the form of eye drops.

Adults: Apply as required, typically in the form of eye drops.

Mechanism of action

Hypromellose acts by forming a viscous gel upon contact with the ocular surface, which helps to retain moisture and protect against irritants. This gel-like property enhances the stability of the tear film and reduces evaporation, thereby alleviating symptoms associated with dry eye conditions.

Pharmacodynamics

The pharmacodynamic effects of hypromellose are primarily related to its ability to mimic natural tears, providing lubrication to the ocular surface. This lubrication reduces friction during blinking and maintains corneal hydration, which is critical for ocular comfort and health. Its high viscosity also contributes to prolonged retention time on the eye surface.

Pharmacokinetics

Hypromellose is administered topically as eye drops and is not significantly absorbed systemically. The retention time of hypromellose on the ocular surface is enhanced due to its viscosity, allowing for extended relief of dry eye symptoms. The elimination of hypromellose occurs primarily through drainage from the eye and dilution by the natural tear fluid.

Adverse effects

• Temporary visual disturbance
• Eye irritation

Precautions

• Should not be used during contact lens wear
• Use with caution in patients with known hypersensitivity to any component of the formulation

Pregnancy

Hypromellose is generally considered safe for use during pregnancy. However, it should be used only if clearly needed and after consulting a healthcare provider.

Breast-feeding

Hypromellose is unlikely to affect breastfed infants when used as directed, but consultation with a healthcare provider is advisable.

Storage

Store in a cool, dry place away from direct sunlight. Once opened, use within a specified period as indicated on the packaging.

Formulations

• {'name': 'Teardew', 'concentration': '0.3%', 'form': 'eye drops', 'volume': '10 ml'}
• {'name': 'Xailin Hydrate', 'concentration': '0.3%', 'form': 'eye drops', 'volume': '10 ml'}
• {'name': 'AacuLose', 'concentration': '0.3%', 'form': 'eye drops', 'volume': '10 ml'}
• {'name': 'Artelac', 'concentration': '0.32%', 'form': 'eye drops', 'volume': '10 ml'}
• {'name': 'Lacrilube', 'concentration': '2 mg/g', 'form': 'eye ointment', 'volume': '3.5 g'}
• {'name': 'Celluvisc', 'concentration': '1%', 'form': 'eye drops', 'volume': '0.4 ml unit dose'}

Indications

• Hypertension
• Angina pectoris (prophylaxis)

Dosage

Children: Not licensed for use in children.

Adults: Initially 5 mg three times a day, which may be adjusted according to response, with a typical maintenance dose of 10-20 mg three times a day. For modified-release formulations, the initial dose is often 20 mg twice daily.

Mechanism of action

Nifedipine blocks voltage-gated L-type calcium channels in vascular smooth muscle and myocardial cells. This action prevents calcium ions from entering the cells during depolarization, reducing peripheral arterial resistance and dilating coronary arteries. This results in lowered blood pressure and increased oxygen delivery to the heart, alleviating angina symptoms. The mechanism by which nifedipine inhibits calcium influx is not completely understood, but it is believed to involve interference with ion-control gating mechanisms of the calcium channels.

Pharmacodynamics

Nifedipine is an inhibitor of L-type voltage-gated calcium channels, which reduces blood pressure and increases oxygen supply to the heart. The immediate-release formulations require dosing three times daily due to their shorter duration of action. The typical daily dose ranges from 10 to 120 mg, with careful monitoring for excessive hypotension and potential angina exacerbation.

Pharmacokinetics

Nifedipine is rapidly absorbed following oral administration, with peak plasma concentrations typically occurring within 30 minutes to 2 hours for immediate-release forms. Its bioavailability is affected by first-pass metabolism, and it is extensively metabolized in the liver. The half-life of nifedipine varies, but it generally ranges from 2 to 5 hours. The drug is primarily excreted as metabolites in the urine, with only a small fraction excreted unchanged.

Contra-indications

• Cardiogenic shock
• Aortic stenosis
• Severe maternal hypotension
• Fatal fetal hypoxia in pregnancy

Adverse effects

• Constipation
• Malaise
• Oedema
• Allergic reactions
• Angioedema
• Hypotension
• Reflex tachycardia

Interactions

• Grapefruit juice (severe increase in exposure)
• Rifampicin (severe decrease in exposure)
• Enzalutamide (moderate decrease in exposure)
• Dronedarone (moderate increase in exposure)
• Antifungal azoles (moderate increase in exposure)
• Miconazole (moderate increase in exposure)
• Cobicistat (moderate increase in exposure)
• Crizotinib (moderate increase in exposure)
• Dabrafenib (moderate decrease in exposure)
• Idelalisib (moderate increase in exposure)

Precautions

• Monitor blood pressure and heart rate regularly
• Use with caution in patients with significant left ventricular dysfunction
• Avoid excessive decrease in blood pressure
• Consider initial low doses in patients with renal impairment

Pregnancy

May inhibit labour; not to be used in multiple pregnancies unless no other acceptable alternative.

Breast-feeding

Manufacturer advises to avoid; present in breast milk.

Storage

Store at room temperature, away from moisture and heat.

Formulations

• Immediate-release capsules
• Modified-release formulations
• Oral suspension
• Solution for infusion

Indications

• Constipation
• Dietary fiber supplementation
• Irritable bowel syndrome
• Diverticular disease
• Weight management

Dosage

Children: Refer to appropriate guidelines for specific dosage; generally taken with adequate fluid intake.

Adults: Refer to appropriate guidelines for specific dosage; generally taken with adequate fluid intake.

Mechanism of action

Cellulose acts primarily as a bulk-forming laxative. It absorbs water in the intestines, which increases stool bulk and stimulates peristalsis, thus facilitating bowel movements. Additionally, cellulose is not digestible by human enzymes, leading to fermentation by gut bacteria, which may enhance gut health and alter gut microbiota composition.

Pharmacodynamics

Cellulose increases stool weight and frequency of bowel movements. It works by retaining water in the intestines, leading to softer stools and improved passage through the gastrointestinal tract. The bulking effect of cellulose can help alleviate constipation and promote overall digestive health. It may also play a role in cholesterol reduction and glycemic control through its effects on digestion and absorption of nutrients.

Pharmacokinetics

Cellulose is not absorbed into the bloodstream due to its indigestible nature. Instead, it passes through the gastrointestinal tract, where it adds bulk to the stool. Its fermentation by colonic bacteria produces short-chain fatty acids, which may have beneficial effects on colon health. The onset of action for cellulose as a laxative can vary but is generally within 24 to 72 hours after ingestion.

Adverse effects

• Bloating
• Flatulence
• Diarrhea
• Abdominal discomfort

Precautions

• Use with caution in patients with a history of gastrointestinal disorders.
• Monitor for potential allergic reactions in sensitive individuals.

Pregnancy

Cellulose is generally considered safe during pregnancy as it is a non-toxic, indigestible fiber.

Breast-feeding

Cellulose is also considered safe during breastfeeding; it is excreted in breast milk in negligible amounts.

Storage

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

Formulations

• Powder
• Capsules
• Tablets
• Granules

Indications

• Monitoring respiratory function
• Assessment of metabolic status
• Management of respiratory acidosis
• Management of respiratory alkalosis

Dosage

Children: Dosing for interventions related to carbon dioxide levels in pediatric patients should be guided by clinical protocols and the BNF for Children.

Adults: Dosing for interventions related to carbon dioxide levels is typically based on clinical assessment and individual patient needs. Refer to clinical guidelines for specific scenarios.

Mechanism of action

Carbon dioxide acts primarily as a signaling molecule in the body, influencing respiratory drive and blood pH. It is produced during cellular respiration and is a critical component of the bicarbonate buffering system, which helps maintain acid-base homeostasis. Elevated levels of CO2 in the blood stimulate ventilation in the lungs, increasing the rate of gas exchange and facilitating the removal of excess CO2.

Pharmacodynamics

The pharmacodynamic effects of dioxides, particularly carbon dioxide, are closely related to its concentration in the blood. As CO2 levels increase, it leads to respiratory acidosis, which can stimulate the respiratory centers in the brain to increase ventilation. Conversely, low levels of CO2 can cause respiratory alkalosis, potentially leading to decreased respiratory drive. CO2 also plays a role in vasodilation and can affect blood flow and pressure through its influence on smooth muscle tone.

Pharmacokinetics

Carbon dioxide is produced endogenously during metabolic processes and is transported in the bloodstream primarily in three forms: dissolved in plasma, as bicarbonate ions (HCO3-), and bound to hemoglobin. The half-life of CO2 in the bloodstream is very short due to its rapid exchange with alveolar gas in the lungs. The elimination of CO2 occurs through exhalation, making it a dynamic component of respiratory physiology.

Pregnancy

Data on the effects of dioxide during pregnancy are limited. Caution is advised due to potential risks associated with exposure.

Breast-feeding

Limited data are available regarding the excretion of dioxide in human milk. Caution is recommended.

Storage

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

Indications

• Iron deficiency anemia
• Chronic blood loss
• Nutritional iron deficiency
• Pregnancy-related anemia

Dosage

Children: Refer to the BNF for Children for specific dosing information as it may vary based on the formulation and clinical context.

Adults: Refer to the BNF for specific dosing information as it may vary based on the formulation and clinical context.

Mechanism of action

Ferric ions participate in various biological processes, including oxygen transport and electron transfer. They facilitate the formation of hemoglobin in red blood cells, allowing for efficient oxygen delivery throughout the body. Ferric compounds can also promote the absorption of iron from the gastrointestinal tract by providing a more bioavailable form of iron.

Pharmacodynamics

Ferric compounds exhibit their effects primarily through the restoration of iron levels in the body. This leads to improved synthesis of hemoglobin and overall enhancement of oxygen-carrying capacity. The pharmacological action is dose-dependent, with higher doses leading to more pronounced effects on hemoglobin levels and erythropoiesis. Additionally, ferric ions can influence various metabolic pathways involved in cellular respiration and energy production.

Pharmacokinetics

Ferric is absorbed in the gastrointestinal tract, with absorption rates influenced by dietary factors and the presence of other substances in the gut. Once absorbed, ferric ions are transported in the bloodstream bound to transferrin, a transport protein. The body regulates iron levels primarily through absorption rather than excretion, and excess iron can be stored in the liver, spleen, and bone marrow. The elimination of ferric compounds is generally slow, as they are incorporated into various biological systems or stored for future use.

Contra-indications

• Hypersensitivity to ferric compounds
• Iron overload conditions such as haemochromatosis or haemosiderosis
• Chronic liver disease
• Active peptic ulcer disease

Adverse effects

• Gastrointestinal disturbances including nausea, vomiting, and constipation
• Diarrhea
• Abdominal pain
• Black stools
• Allergic reactions including rashes and anaphylaxis
• Staining of teeth (with oral formulations)

Interactions

• Antacids may reduce the absorption of oral ferric preparations
• Tetracyclines and quinolone antibiotics may have reduced absorption when taken with iron
• Ascorbic acid may enhance the absorption of iron

Precautions

• Caution in patients with a history of gastrointestinal disease
• Monitor for signs of iron overload in patients receiving repeated doses
• Use with caution in patients with renal impairment

Pregnancy

Ferric compounds are generally considered safe in pregnancy when used as directed to treat iron deficiency, but should be used under medical supervision.

Breast-feeding

Ferric compounds are excreted in breast milk in small amounts, usually considered safe but should be used under medical supervision.

Storage

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

Formulations

• Oral tablets
• Oral solution
• Intravenous injection

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

• Ophthalmic solutions
• Topical formulations
• Oral solid dosage forms
• Stabilizer in various pharmaceutical preparations

Dosage

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

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

Mechanism of action

Hydroxypropylcellulose functions primarily as a viscosity-increasing agent. When dissolved in water, it forms a gel-like consistency that helps to stabilize formulations. Its mechanism is related to its ability to create a hydrated film, which can enhance the retention of active ingredients and improve the delivery of medications to the targeted area, particularly in ocular applications.

Pharmacodynamics

The pharmacodynamic properties of hydroxypropylcellulose are primarily related to its physical characteristics rather than specific receptor interactions. It exhibits properties such as gel formation and moisture retention, which can enhance the stability and effectiveness of drug formulations. Its viscosity can influence the release rates of active pharmaceutical ingredients, thereby affecting the overall therapeutic effect.

Pharmacokinetics

Hydroxypropylcellulose is not systemically absorbed when used in pharmaceutical applications, as it acts locally at the site of application. Its pharmacokinetics involves dissolution and gel formation in the presence of water, with no significant metabolic pathways or excretion processes, given its large molecular structure. The duration of action is primarily influenced by the formulation and the concentration used.

Pregnancy

Hydroxypropylcellulose is generally considered safe for use during pregnancy as it is not systemically absorbed. However, it should be used only when clearly needed.

Breast-feeding

Hydroxypropylcellulose is not absorbed systemically and is considered safe for use during breastfeeding.

Storage

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

Formulations

• Ophthalmic solutions
• Topical gels
• Oral capsules
• Powders for reconstitution

Indications

• Constipation
• Bowel preparation for diagnostic procedures (e.g., colonoscopy)

Dosage

Children: For children, macrogol is typically used at a dose of 0.5 to 1 g/kg per day, not exceeding 17 g per day, depending on the child's age and condition. Refer to the BNF for Children for detailed pediatric dosing guidance.

Adults: Typical adult dosing for constipation is 8.4 grams of macrogol powder dissolved in water, taken once daily. For bowel preparation, specific dosing regimens may vary, and it is essential to follow product instructions or medical advice.

Mechanism of action

Macrogol works as an osmotic agent, drawing water into the bowel lumen through osmosis. This increased water content softens the stool, making it easier to pass. The presence of macrogol in the intestine increases the volume and viscosity of the stool, stimulating peristalsis and facilitating bowel evacuation.

Pharmacodynamics

Macrogol's laxative effect is dose-dependent, with higher doses generally resulting in more significant bowel movement stimulation. It is not absorbed systemically, which minimizes potential side effects and interactions. The osmotic effect leads to an increase in intraluminal pressure and stool volume, contributing to effective evacuation.

Pharmacokinetics

Macrogol is largely non-absorbed in the gastrointestinal tract, which allows it to exert its effects locally within the bowel. Due to its high molecular weight, it remains in the intestinal lumen, where it facilitates water retention. Elimination occurs through feces, as it is not metabolized by the body.

Pregnancy

Macrogol can be used during pregnancy if necessary, but caution should be exercised and medical advice sought.

Breast-feeding

Macrogol is generally considered safe to use during breastfeeding.

Storage

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

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.

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.

Indications

• Orthopedic implants
• Dental implants
• Prosthetic devices
• Surgical instruments

Mechanism of action

Titanium does not have a specific mechanism of action as it is not a drug in the traditional sense. Instead, its biocompatibility allows it to integrate with biological tissues without eliciting significant immune responses, making it suitable for use in implants and prosthetic devices. The presence of titanium ions can influence biological processes, including cell proliferation and differentiation.

Pharmacodynamics

Titanium itself does not exhibit pharmacodynamics as it is not administered as a drug. Its interactions within biological systems are primarily mechanical and structural, providing support and stability in orthopedic and dental applications. The biocompatibility of titanium allows for favorable tissue integration and reduced rejection rates compared to other materials.

Pharmacokinetics

As titanium is not a pharmacological agent, traditional pharmacokinetic parameters such as absorption, distribution, metabolism, and excretion do not apply. Titanium is typically utilized in solid forms, such as implants, where it remains localized and does not undergo metabolism or systemic circulation.

Pregnancy

There is limited data on the use of titanium during pregnancy. Consult a healthcare professional before use.

Breast-feeding

There is limited data on the excretion of titanium in breast milk. Consult a healthcare professional before use.

Storage

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

Mechanism of action

Nifedipine blocks voltage gated L-type calcium channels in vascular smooth muscle and myocardial cells. This blockage prevents the entry of calcium ions into cells during depolarization, reducing peripheral arterial vascular resistance and dilating coronary arteries. These actions reduce blood pressure and increase the supply of oxygen to the heart, alleviating angina. The principal physiologic action of nifedipine is to inhibit the transmembrane influx of extracellular calcium ions across the membranes of myocardial cells and vascular smooth muscle cells, without changing serum calcium concentrations. Calcium plays important roles in the excitation-contraction coupling processes of the heart and vascular smooth muscle cells and in the electrical discharge of the specialized conduction cells of the heart. The membranes of these cells contain numerous channels that carry a slow inward current and that are selective for calcium. Activation of these slow calcium channels contributes to the plateau phase (phase 2) of the action potential of cardiac and vascular smooth muscle cells. The exact mechanism whereby nifedipine inhibits calcium ion influx across the slow calcium channels is not known, but the drug is thought to inhibit ion-control gating mechanisms of the channel, deform the slow channel, and/or interfere with release of calcium from the sarcoplasmic reticulum. By inhibiting calcium influx, nifedipine inhibits the contractile processes of cardiac and vascular smooth muscle, thereby dilating the main coronary and systemic arteries. Nifedipine is a peripheral arterial vasodilator which acts directly on vascular smooth muscle. The binding of nifedipine to voltage-dependent and possibly receptor-operated channels in vascular smooth muscle results in an inhibition of calcium influx through these channels. Stores of intracellular calcium in vascular smooth muscle are limited and thus dependent upon the influx of extracellular calcium for contraction to occur. The reduction in calcium influx by nifedipine causes arterial vasodilation and decreased peripheral vascular resistance which results in reduced arterial blood pressure.

Pharmacodynamics

Nifedipine is an inhibitor of L-type voltage gated calcium channels that reduces blood pressure and increases oxygen supply to the heart. Immediate release nifedipine's duration of action requires dosing 3 times daily. Nifedipine dosing is generally 10-120mg daily. Patients should be counselled regarding the risk of excessive hypotension, angina, and myocardial infarction.

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

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

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.