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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)

Effect of NNMT inhibitor on adipocyte differentiation quantitated with oil red O staining 3T3-L1 cells were cultured in 60 mm diameter dishes (8.410 4 cells/dish) and treated with NNMT inhibitor dissolved in culture media with/without adipogenic factors (1 mM IBMX, 1 M dexamethasone, 10 g/ml of insulin) during each of the scheduled media changes during the differentiation process (described above)

doi: 10.1006/abbi.1996.9867

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Green chemistry with selenium reagents: development of efficient catalytic reactions