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Other relevant repair/oxidative stress protection mechanisms of NAC may also be relevant and worth exploring [33], including mechanisms by which NAC scavenges free radicals [34], induces neurogenesis [35], reduces mitochondrial apoptosis [36], reduces glutamatergic neurotransmission [29], and chelates metals as a form of oxidative stress protection [37]

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4-Hydroperoxycyclophosphamide (4HC) resistance in human CML line B5-180

Plausibly, this non-specificity might contribute to contradictory effects observed in different cell types (Wang et al., 2009)