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The picture that emerges from these experiments is that endogenous GSH is not just an inhibitor of inflammation, but it is required to allow a proper response to infection, and direct the migration of inflammatory PMN away from the lung, where they cause ARDS, and towards the site of infection, where they kill bacteria (Figure 6)

It is known to be particularly reaction with histidine, which often located at the active sites of SODs, so singlet molecular oxygen may result in prevention of the activities of those enzymes including CATs and GPXs