PCD occurs via a number of different mechanisms, e.g. caspase-dependent or independent, however, in all eukaryotes it is thought to be correlated with high levels of reactive oxygen species (ROS). ROS can either be generated exogenously through respiration or originate from exogenous sources such as exposure to hydrogen peroxide (H 2 O 2 ), superoxide anions or hydroxyl radicals. Excessive ROS results in damage of cellular components (DNA, lipids and proteins), cell cycle arrest, ageing and finally cell death (24) . Cells have developed a complex network of defence mechanisms, both enzymatic and non-enzymatic, against adverse consequences of oxidative stress (25) . Non-enzymatic system comprises a set of small molecules acting as ROS scavengers (e.g. glutathione, thioredoxin, glutaredoxin and ascorbic acid), whereas enzymatic system eliminates oxygen radicals by the action of specialized cytosolic or mitochondrial enzymes (e.g. catalases, superoxide dismutases, glutathione peroxidases and thioredoxin peroxidases) (25) . Most genes encoding components of these systems are induced in response to oxidative stress and are under transcriptional control of specific factors, for example Yap1, Msn2/Msn4 and Skn7 in budding yeast (26) . However, it appears that there is no general oxidative stress response. In S. cerevisiae, different response pathways are triggered by specific oxidants and different genes are involved in maintaining efficient cellular resistance to various sources of ROS (1, 2) . Interestingly, recent genomic approaches to identify these genes showed that strains lacking proteins which function in RNA metabolism were oversensitive to oxidative stress (1,2). These included genes encoding rRNA helicases (Dbp3, Dbp7), rRNA processing factors (Nop12, Nsr1), mRNA deadenylases (Ccr4, Pop2) and several mitochondrial RNA splicing components (2, 27) . This indicates that RNA processing and degradation may have a role in cellular response to ROS.