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Thirty-two male albino rats were divided into four groups: the control group, the N-acetylcysteine (NAC) group orally as effervescent instant sachets with a concentration of 200\u00a0mg dissolved in distilled water and dosage was 200\u00a0mg\/kg body weight freshly prepared, the cadmium chloride (CdCl<jats:sub>2<\/jats:sub>) group (treated with 3\u00a0mg\/kg orally), and the N-acetylcysteine (NAC)\u2009+\u2009cadmium chloride group (treated with 200\u00a0mg\/kg orally post to CdCl<jats:sub>2<\/jats:sub>) for 60\u00a0days. The NAC alone did not make notable changes in most of the parameters. The CdCl<jats:sub>2<\/jats:sub> alone, compared to control, induced significant alterations in oxidative stress markers (increment in lipid peroxidation (LPO) and nitric oxide (NO)) and antioxidant defense system (decrement in superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx)), which resulted in a downregulation of pro-apoptotic Bcl2-associated X protein (Bax) and caspase-3 and upregulation of anti-apoptotic B-cell leukemia\/lymphoma 2 (Bcl2) protein as well as the survival fate of hepatic cells. Post-administration of NAC to CdCl<jats:sub>2<\/jats:sub> resulted in a reduction in oxidative stress markers, shifting of cells from the <jats:italic>G<\/jats:italic><jats:sub>2<\/jats:sub>\/<jats:italic>M<\/jats:italic> phase to the <jats:italic>G<\/jats:italic><jats:sub>0<\/jats:sub>\/<jats:italic>G<\/jats:italic><jats:sub>1<\/jats:sub> inhibiting signal-regulated kinase activation, and impairment of the anti-apoptotic signaling pathway when compared to the CdCl<jats:sub>2<\/jats:sub> group alone. Accordingly, the Bcl2\/Bax ratio was reduced to 1.17-fold change, as an adaptive process to hepatic tissue injury. 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