The toxicity of the European yew (
Taxus baccata, family
Taxaceae), a shrub that grows plentifully in the territory of the Czech Republic, has been known since ancient times and was known to the ancient Celts. The European yew contains several different compounds, such as phenolic compounds (for example, 3,5-dimethoxyphenol) together with non-alkaloidal diterpenoids (for example, 10-deacetylbaccatin III), alkaloidal diterpenoids (for example, paclitaxel, taxine B), flavonoids (for example, myricetin) and bioflavonoids (for example, bilobetin); some of these are considered as relatively highly toxic [
1]. Descriptions of poisoning in the literature are quite rare. The rapid, lethal process of poisoning does not usually allow enough time for studying biochemical and electrophysiological changes. The plant’s poisonous parts include needles, bark and wood, but not the fruit (red berries). The taxine alkaloids (for example, taxine A, 2-deacetyltaxine A, isotaxine B, 1-deoxytaxine B) derived from
p-dimethylaminohydroxycinnamic acid are the effective poisons of the yew [
1]. In chemical terms, the compound is structurally related to veratrine, and the presence of an unsaturated lactone group makes this group of alkaloids similar to digitalis. Poisoning with the latter may be falsely diagnosed during a toxicological examination. Cardiac disturbances after intoxication by yew are ascribed mainly to the alkaloids paclitaxel and taxine B, affecting sodium/calcium permeability in cells [
2]. The taxine alkaloid is absorbed through the digestive tract very rapidly, and the signs of poisoning manifest themselves after 30 to 90 minutes. An infusion made from 50 to 100g of needles is considered to be fatal [
3‐
5], as no antidote is known.