In the present studies we tested the hypotheses that: 1) the expression levels of SSAT and SMOX increase in response to cisplatin treatment; 2) cisplatin-induced AKI is in part mediated via enhanced activity of polyamine catabolic enzymes and through generation of H2O2 and aminoaldehydes (e.g. 3-aminopropanal, acetyl-3-aminopropanal and acrolein); and 3) Increased polyamine catabolism activates ERSR, a pathway that is critical to the mediation of cell injury, tissue damage and organ dysfunction. Here, SAT1 is linked to acute kidney injury.