The reason why treatment with some oxidative agents but not others produce fragmented RNA is not entirely clear, however, it is known that different chemicals induce specific responses leading to expression of distinct sets of genes (1, 2) , and possibly only a few activate pathways that involve RNA destruction. Our results suggest that rRNA degradation phenotype most likely accompanies apoptosis, and only apoptosis-inducing oxidants result in rRNA decay, whereas cell death caused by others probably occurs via a different mechanism. Another question is why each apoptotic stimuli resulted in slightly different set of cleavage products. Those which were mapped for treatment with H 2 O 2 and in aging cells illustrate that cleavages often occur in loops and bulges in closely located regions within the 25S rRNA, or rather within the accessible RNA elements in the compact RNP structures. The difference in cleavage patterns could be due to stress-induced subtle or severe alterations in ribosome particles that change the local accessibility of the rRNA components presented for cleavage. Alternatively, if rRNA decay is indeed carried out by more than one nuclease, these differences may reflect varying enzyme specificities in each death-inducing condition. It is also possible that somehow different set of nucleases is activated or recruited to rRNA substrates during apoptosis triggered by oxidative stress, acetic acid treatment and ageing.