Objective To examine the role of Cd-induced reactive oxygen species(ROS)generation in the apoptosis of neuronal cells.Methods Neuronal cells(primary rat cerebral cortical neurons and PC12 cells)were incubated with or without Cd post-pretreatment with rapamycin(Rap)or N-acetyl-L-cysteine(NAC).Cell viability was determined by MTT assay,apoptosis was examined using flow cytometry and fluorescence microscopy,and the activation of phosphoinositide 3’-kinase/protein kinase B(Akt)/mammalian target of rapamycin(m TOR)and mitochondrial apoptotic pathways were measured by western blotting or immunofluorescence assays.Results Cd-induced activation of Akt/m TOR signaling,including Akt,m TOR,p70 S6 kinase(p70 S6K),and eukaryotic initiation factor 4E binding protein 1(4E-BP1).Rap,an m TOR inhibitor and NAC,a ROS scavenger,blocked Cd-induced activation of Akt/m TOR signaling and apoptosis of neuronal cells.Furthermore,NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein(Bcl-2/Bax)ratio,release of cytochrome c,cleavage of caspase-3 and poly(ADP-ribose)polymerase(PARP),and nuclear translocation of apoptosis-inducing factor(AIF)and endonuclease G(Endo G).Conclusion Cd-induced ROS generation activates Akt/m TOR and mitochondrial pathways,leading to apoptosis of neuronal cells.Our findings suggest that m TOR inhibitors or antioxidants have potential for preventing Cd-induced neurodegenerative diseases. Objective To examine the role of Cd-induced reactive oxygen species (ROS) generation in the apoptosis of neuronal cells. Methods Neuronal cells (primary rat cerebral cortical neurons and PC12 cells) were incubated with or without Cd post-pretreatment with rapamycin (Rap) or N-acetyl-L-cysteine ​​(NAC). Cell viability was determined by MTT assay, apoptosis was examined using flow cytometry and fluorescence microscopy, and the activation of phosphoinositide 3’-kinase / protein kinase B (Akt) / mammalian target of Results of Cd-induced activation of Akt / m TOR signaling, including Akt, m TOR, p70 S6 kinase (p70 S6K), and eukaryotic initiation factor 4E binding protein 1 (4E-BP1). Rap, an m TOR inhibitor and NAC, a ROS scavenger, blocked Cd-induced activation of Akt / m TOR signaling and apoptosis of neuronal cells. / Bcl-2 associated X protein (Bcl-2 / Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly (ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G) Akt / m TOR and mitochondrial pathways, leading to apoptosis of neuronal cells. Our findings suggest that m TOR inhibitors or antioxidants have potential for preventing Cd-induced neurodegenerative diseases.