The pathogenesis of influenza virus infection involves virus replication in epithelial cells of the respiratory tract and the degeneration of infected cells resulting from subsequent events.1 Influenza virus induces cellular degeneration following infection of cultured cells in vitro, and the cytopathic effect (CPE) occurs principally through apoptotic cell death.1–10 Influenza virus replication is an essential process for the induction of apoptosis;3–6 however, the precise mechanism of influenza virus-induced apoptosis is unclear. Recently, several reports have described the effect of antioxidants such as pyrrolidine dithiocarbamate (PDTC), N-acetyl-l-cysteine (NAC) and 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (Trolox) on influenza virus-induced apoptosis in terms of the involvement of reactive oxygen species (ROS) in a possible mechanism of apoptosis induction (Table 1).3,7–9,11,12