The anticancer activity of sulforaphane is known to be mediated at least partly by apoptosis induction and associated with the presence of the -N=C=S moiety. The present study explored how oxidation of sulphur in the side chain of sulforaphane affected apoptosis induction to provide the chemical basis of sulforaphane effects. Sulforaphane analogues containing oxidised sulphur (alyssin, sulforaphane, erysolin and alyssin sulfone) exerted a superior growth inhibitory effect compared with sulforaphane analogues with nonoxidised sulphur (erucin and berteroin) in human colon cancer cell lines. Furthermore, erysolin was a more potent inducer of reactive oxygen species (ROS) and apoptosis compared with erucin. Erysolin-induced ROS generation and subsequent apoptosis were inhibited by pretreatment with the antioxidant N-acetyl-cysteine. Erysolin induced caspase-8 activation, while blockade of caspsase 8 activation inhibited apoptosis induced by erysolin. Taken together, sulforaphane analogues with oxidised sulphur were the most efficient apoptosis inducers, likely due to high-level ROS induction.