Intracox Oral

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

Dosage

Children: Refer to specific product guidelines for dosing information, as monoethanolamine is primarily used in industrial applications and as a chemical intermediate rather than a therapeutic agent.

Adults: Refer to specific product guidelines for dosing information, as monoethanolamine is primarily used in industrial applications and as a chemical intermediate rather than a therapeutic agent.

Mechanism of action

Monoethanolamine acts by participating in the biosynthesis of phospholipids. It is involved in the formation of phosphatidylethanolamine and other phospholipids that are crucial for maintaining cell membrane integrity and function. This compound's role in lipid metabolism indicates its significance in cellular signaling and membrane fluidity.

Pharmacodynamics

Monoethanolamine's pharmacodynamic properties are linked to its function as a precursor in the synthesis of phospholipids. These phospholipids play critical roles in cell membrane structure, signaling pathways, and cellular communication. The modulation of phospholipid composition can influence cellular responses to various stimuli, highlighting the compound's importance in cell biology.

Pharmacokinetics

The pharmacokinetics of monoethanolamine are not well-documented in the available literature. However, as a small molecule, it is likely to be absorbed readily and distributed throughout the body. Its metabolic pathways involve conversion into various phospholipids, and it may be excreted as part of these metabolites. Additional studies would be needed to detail its absorption, distribution, metabolism, and excretion (ADME) characteristics.

Pregnancy

There is insufficient data on the use of monoethanolamine in pregnancy. Caution is advised.

Breast-feeding

There is limited information on the effects of monoethanolamine during breastfeeding. Caution is recommended if used.

Storage

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

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

• Coccidiosis
• Protozoan infections

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines.

Mechanism of action

Toltrazuril acts by inhibiting the mitochondrial respiratory chain of protozoa, leading to a disruption of ATP synthesis. This mechanism results in the inhibition of the growth and reproduction of coccidia, particularly Eimeria species, by impairing their energy metabolism.

Pharmacodynamics

Toltrazuril exhibits its effects through selective targeting of the protozoan parasites' mitochondrial functions. The disruption of ATP synthesis results in reduced energy availability for cellular processes, ultimately leading to the death of the parasite. It has a high efficacy against various stages of the coccidian life cycle.

Pharmacokinetics

Toltrazuril is well absorbed after oral administration, with peak plasma concentrations occurring within a few hours. It is extensively metabolized in the liver, with metabolites contributing to its pharmacological activity. The elimination half-life allows for sustained effects against parasitic infections. The drug is primarily excreted via feces.

Pregnancy

There is limited data on the use of toltrazuril in pregnancy. It should only be used if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

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

Storage

Store below 30°C. Protect from light and moisture.

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.