OBJECTIVE: To investigate the mechanism of methamphetamine (METH)-induced toxicity in PC12 cells. METHODS: PC12 cells were treated with METH for 24 h at the doses of 0, 0.5, 1.0, 1.5, 2.0, or 2.5 mmol/L. The morphological changes of the cells were observed under inverted microscope after the treatment. MTT assay and flow cytometry were used to assess the cell viability and apoptotic rates, respectively, and the level of nitric oxide (NO) was measured by enzyme reduction method. RESULTS: The PC12 cells exposed to METH were morphologically featured by cell shrinkage, dendrite disruption and disappearance of cell reticular formation. METH exposure caused a dose-dependent reduction in the cell viability (P<0.01), resulting in also increased cell apoptotic rate and significant elevation of NO in the cell culture supernatant (P<0.05). CONCLUSION: METH exposure induces cytotoxicity and injury of differentiated PC12 cells, leading to decreased cell viability and increased cell apoptosis and NO level. Cell apoptosis and excessive NO production are involved in METH-induced cytotoxicity.
OBJECTIVE: To investigate the mechanism of methamphetamine (METH)-induced toxicity in PC12 cells. METHODS: PC12 cells were treated with METH for 24 h at the doses of 0, 0.5, 1.0, 1.5, 2.0, or 2.5 mmol/L. The morphological changes of the cells were observed under inverted microscope after the treatment. MTT assay and flow cytometry were used to assess the cell viability and apoptotic rates, respectively, and the level of nitric oxide (NO) was measured by enzyme reduction method. RESULTS: The PC12 cells exposed to METH were morphologically featured by cell shrinkage, dendrite disruption and disappearance of cell reticular formation. METH exposure caused a dose-dependent reduction in the cell viability (P<0.01), resulting in also increased cell apoptotic rate and significant elevation of NO in the cell culture supernatant (P<0.05). CONCLUSION:METH exposure induces cytotoxicity and injury of differentiated PC12 cells, leading to decreased cell viability and increased cell apoptosis and NO level. Cell apoptosis and excessive NO production are involved in METH-induced cytotoxicity.