1-Methyl-4-phenyl-pyridinium (MPP+) and 6-hydroxydopamine (6-OHDA) are the predominant neurotoxic agents used in the research of Parkinson's disease (PD). The mTORC2 is a significant signaling pathway whose specific functions and mechanisms remain partially elusive, especially in the context of PD-related oxidative stress. We aimed to determine the interconnection between mTORC2 and oxidative stress in MPP+ and 6-OHDA neurotoxic models of PD. All experiments were performed on the human neuroblastoma cell line, SH-SY5Y. Cells were divided into two groups: control (consists of control cells and cells treated with MPP or 6-OHDA) and NAC group (consists of control cells and cells treated with MPP or 6-OHDA, but pretreated with N-acetylcysteine). MTT assay was used for the determination of cell viability. The activation status of mTORC2 components and downstream targets was determined by immunoblotting. The level of ROS was measured by flow cytometry. We showed that cell viability decreased with increasing concentrations of MPP+ and 6-OHDA, whereas pretreatment with NAC improved cell viability. With NAC pretreatment, the phosphorylated forms of mTOR and Rictor were increased, but the opposite effect was observed in Sin1 and Akt patterns. Also, it has been shown that inhibition of mTORC2 components (Rictor, Sin1 and MLST8) increased the production of ROS. We can conclude that the NAC antioxidative effect ameliorates the MPP+ and 6-OHDA neurotoxic effects on human neuroblastoma cells, leading to a change in mTORC2 activity. However, the order of activation among the members and the specific impact of this process have yet to be elucidated.