The cytotoxicity potentials of methamphetamine (METH) is presumably associated with oxidative stress induced apoptosis, this study therefore, investigated the toxic potentials of METH in neuroblastoma cells and further determined it effects on the mitochondrial activity. Human neuroblastoma SK-N-BE (2) cells cultured in DMEM/F12 were used in this study. The cells were treated acutely with methamphetamine (1, 5, 10, 20, and 50 µg/mL) over 24, and were allowed to recover from METH treatment over 48, 72, and 96 h. Cell viability study was done with Trypanblue exclusion assay. The cell proliferative characteristics of the neuroblastoma cell line were investigated by constructinga cell proliferation curve. Mitochondrial activity was assessed using the XTT Assay. Statistical analysis were done with Graph Pad prism and significant difference were considered at p<0.001, 0.01 and 0.05. The result showed normal growth in the untreated neuroblastoma cell over the 96 h of monitoring. Following treatment with METH, significant decrease in cell growth was observed when treated acutely with 5 and 10 µg/mL METH and allowed till 72 and 96 h recovery period. The SK-N-BE (2) treated with increasing concentration of METH showed no significant difference in cell viability over the recovery period from METH exposure. Toxicity of SK-N-BE (2) cells was only observed when treated with 10 µg/mL of METH. Significant decrease in mitochondria activity was observed when the cells were treated with 5, 10, 20, and 50 µg/mL METH and allowed till 72 h recovery. The result showed that METH is cytotoxic to the SK-N-BE (2) cells and the mechanism of toxicity might be associated with inhibition of mitochondrial activity.