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In the final phase, cell death mechanisms are activated, marked by increased cleavage of caspase three and reduced synthesis of Bcl-2

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1) that can reduce singlet oxygen, superoxide anions, hydroxyl radicals, and hydrogen peroxide through an ene-diol group on its lactone ring (Shamberger 1984

Free cystine accumulated in cancer cells forms a water-insoluble toxic crystal, often leading to cell damage (i.e., disulfide stress) [48]

Many studies have shown the protective effects of NAC for neonatal animals immune challenged with bacterial lipopolysaccharide (LPS) endotoxin, particularly studies involving piglets [13,14]

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