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However, in glutathione synthetase deficiency, because the activity of gamma-glutamyl-cysteine synthetase is regulated via feedback inhibition by glutathione, gamma-glutamyl-cysteine and then L-5-oxoproline are overproduced, resulting in the metabolic acidosis and urinary excretion of this compound at levels several hundred-fold above normal (71

These final inflammation execution pathways turn on neutrophils via the receptor CXCR2 and other pathways ( Figure 1 - 11 )

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When DQ reacts with cysteine, cysteinyl dopa is generated, which is oxidized to cysteinyl DQ and enters the pheomelanin synthesis pathway