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They suggested an agonist-induced mechanism whereby the addition of GSSG to platelets generated sulfhydryls in the subunit of the IIb 3 fibrinogen receptor [30]

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this is probably due to the high CMFDA fluorescence in the perinuclear area, which could be explained by the fact that BSO, at the concentrations used in this work, is unable to deplete mitochondrial GSH [34], [35]