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In rats, GCLC has a Km for glutamate that is about 10-fold higher than that of the GCL holoenzyme, which is higher than the cellular glutamate concentration in most tissues GCL is specific for the glutamyl moiety and is regulated physiologically by: (a) non-allosteric feedback competitive inhibition by glutathione (GSH) (Ki = 2.3 mM) which involves binding of GSH to the glutamate and another site on the enzyme [8, 9] and (b) availability of its precursor, cysteine [1]
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it is frequently suggested for long-term deficiency cases