The more recent experimental works on the chemistry, industrial uses and general toxicity (with particular reference to liver cell injury) of allyl alcohol (AA) have been briefly reviewed. AA is inactive per se and its toxic expression is modulated by its alcohol dehydrogenase (ADH) oxidation to form acrolein, which is responsible for the hepatotoxic action. The toxicity of the alcohol (or its metabolite acrolein) is dependent on the concentration of glutathione (GSH). After severe depletion of GSH, the reactive metabolite of AA can bind to essential sulfhydryl groups in the cellular macromolecules, leading to structural and functional modifications which can be responsible for cell death. In this case the appearance of lipid peroxidation could be merely the consequence of the death. GSH synthesis precursors exert a protective role in AA intoxication. The significance of calcium modifications in the course of AA toxicity is still under debate.