Warm ischemia produces DNA damage which is characterized by both single- and double-strand breaks with 5'-PO4 and 3'-OH ends. In contrast, cold ischemia produces mostly single-strand breaks for the first 60 hr and then, abruptly, double-strand damage is produced. Cold ischemia produces both 5'-OH and 5'-PO4 termini, but 5'-OH ends do not appear until after 24 hr of storage. Cold ischemia, also produces 3'-PO4 ends but we have not found any 3'-OH termini. Mechanisms for DNA degradation during warm and cold ischemia are presented to account for these results. It is suggested that damage to the genetic code may be prevented if degradation of the DNA can be confined to the production of the easily repairable 5'-PO4/3'-OH opposed ends.