Classically, aconite binds avidly and induces direct confirmation change to open voltage-gated sodium channels by binding site two of the alpha-subunit, with increased preferential binding to highly active channels, which promotes persistent channel opening, enhancing intracellular and, maintaining membrane depolarisation. The structure-activity relationship of aconite is yet to be fully elucidated. Aconite’s half-life (t 1/2) exhibits significant inter-individual variability up to sixteen hours but also variation between other alkaloids within the same family. Aconite alkaloids undergo elimination by first-order kinetics primarily via renal excretion, with a minor pathway involving cytochrome P450 (CYP 3A). The effects of poisoning are classically dose related. Poisoning, with myocardial complications, usually develops within 15-30 minutes following ingestion of the plant leaves or roots. Following enteral absorption, aconite mediates a range of cellular effects via voltagegated sodium channels. Presentation relates not only to the site of absorption of aconite but also plasma concentration of active alkaloids, which varies within the individual parts of plants such as their roots or leaves but also between plants and the processing techniques used during agriculture.Īconite’s pharmacokinetic data has been clarified by several studies. However, only a few cases have been described in western literature in the past twenty years, despite being one of the most toxic plants in the UK.
It is derived from the plant Aconitum napellus, also known as Monkshood or Wolfsbane. Chinese herbalists have actively used aconite for centuries for the treatment of muscular-skeletal disorders due to its analgesic and anti-inflammatory properties. Aconitum is a genus of over two hundred species of flowering plants which contain active ingredients containing aconite and the related alkaloids, lycaconitine and napelline.
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