• Metabolism: Halothane is metabolized in the liver, primarily by CYP2E1, and to a lesser extent by CYP3A4 and CYP2A6.
• Uses/Sources: For the induction and maintenance of general anesthesia
• Health Effects: Damage or injury to the liver.
• Symptoms: Asymptomatic - mild liver damage, nausea, vomitting, abdominal pain, loss of appetite.
• Treatment: In the event of overdosage, or what may appear to be overdosage, drug administration should be stopped, and assisted or controlled ventilation with pure oxygen initiated. There is no specific antidote. Treatment should be aimed at maintaining respiratory function (by moving the patient to fresh air or inserting an emergency airway with respiratory support) and cardiovascular function. Cases of internal ingestion must be treated symptomatically. (L1712)
• Route of Exposure: inhalation

Halothane causes general anaethesia due to its actions on multiple ion channels, which ultimately depresses nerve conduction, breathing, cardiac contractility. Its immobilizing effects have been attributed to its binding to potassium channels in cholinergic neurons. Halothane's effect are also likely due to binding to NMDA and calcium channels, causing hyperpolarization. Halothane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Halothane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. Also appears to bind the D subunit of ATP synthase and NADH dehydogenase. Halothane also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor and the glycine receptor.