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In our previous study, we detected that NAC inhibited the migratory capacity of endometriotic cells, suppressed cell proliferation, and induced ER stress, suggesting a potential mechanism through which NAC exerts its therapeutic effects 20

b-d , HCC-1806 cells were grown in control media or cystine-free (n = 8 technical replicates from 2 independent experiments

Consequently, our data support the idea that the OMM is permeable for glutathione (GSH diffusing into the IMS, or GSSG diffusing out) under the conditions investigated

Published animal studies generally report mild tolerability profiles with limited major adverse effects [1]