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Such an increase in the mRNA levels of the catalytic subunit of -GCS was paralleled by a greater mucosal synthetic GSH capacity determined from either cysteine or -glutamylcysteine used as the sulfur aminoacid in the presence of glycine and glutamate and ATP as described (Fernndez-Checa and Kaplowitz, 1990), indicating an increase in the activity of -GCS following TNBS+ethanol administration (not shown)

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These two conditions although vastly different, share common symptoms, clinical manifestations, pathways and genetic and epigenetic factors and regulators [10, 39]

Thus, NMO can be classified as a primary astrocytopathy