Reactive oxygen species (ROS) mediate the fine balance between cellula
r physiology and pathophysiology, Accordingly it is not surprising tha
t cellular redox homeostasis is disrupted by shock events related to i
schemia-reperfusion and inflammation. ROS may initiate as well as ampl
ify the shock cellular insult in a number of ways which include import
ant contributions to inflammation as well as lytic and apoptotic cell
death. In addition, ROS in the setting of shock represent important an
tecedents to cellular proliferation, differentiation, and adaptation b
y virtue of altered transcription and translation of antioxidant enzym
es, stress proteins, and a variety of cytokines, It is likely that an
eventual important biochemical therapeutic goal in the setting of shoc
k will involve re-establishing cellular redox homeostasis not only to
ensure cellular structural integrity, but also to re-establish normal
secondary cellular signal transduction mechanisms.