Hexachloronaphthalene Induces Mitochondrial-Dependent Neurotoxicity via a Mechanism of Enhanced Production of Reactive Oxygen Species

Figure 6

The role of mitochondria in PCN67-induced toxicity. (a) For measuring mitochondrial membrane potential, differentiated PC12 cells were cultured in the presence of PCN67 for 72 h and then loaded with TMRE (25 nM) for 30 min. TMRE-loaded cells were analyzed for fluorescence intensity using flow cytometry. Individual data points are shown. (b) Partial prevention of PCN67-induced death by Ru360. Ru360 was added 30 min before PCN67 treatment, and the viability was measured 72 h after. (c) Viability assessment of cells cultured in the presence of glucose (25 mM) or galactose (10 mM) supplemented RPMI for 5 days and then treated with PCN67 for 24 h. (d) PCN67-induced cell death is not inhibited by cyclosporine A (CsA). Differentiated PC12 cells were cotreated with PCN67 and CsA, and the viability was assessed 72 h later. and .

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