Abstract Previously labeled smooth-membranes, but not rough membranes, of the endoplasmic reticulum obtained from ischemic rat liver cells lose their radioactivity during long-duration ischemia that will ultimately cause cell death and necrosis. In the period following the re-establishment of the blood supply, irrespective of the duration of previous ischemia, smooth membranes recover their normal levels of radioactivity; at the same time, the specific radioactivity of the rough membranes shows a consistent decline. In post-ischemic livers, de-novo synthesis of membrane protein shows a lag phase of about 2 hours, and is then normally resumed in reversibly injured liver cells; it does not recover appreciably in cells eventually committed to necrosis. In agreement with this observation labeling of the nascent peptide chains on post-ischemic liver ribosomes recovers, after a lag period, only when cells have not been injured to death. Amino acid pools, expanded in ischemic livers, return to normal in both reversibly and irreversibly injured cells and in the former ones normal amino acid concentrations are attained at a time when synthesis of nascent chains is still impaired. These results seem to suggest that flow of the label along the membranes and size of the amino acid pools are not related to the occurrence of cell necrosis; on the contrary, synthesis of nascent peptide chains and of intrinsic membrane protein are better correlated with the final destiny of the cell and their resumption may be tentatively interpreted as the beginning and the necessary prerequisite of cell repair after injury.