Chloramphenicol Mitigates Oxidative Stress by Inhibiting Translation of Mitochondrial Complex I in Dopaminergic Neurons of Toxin-Induced Parkinson’s Disease Model

Figure 2

CP effectively reduced PQ recycling and decreased total ROS levels in SN4741 cells by inhibiting ROS production. (a–c) SN4147 cells were treated with 10 μg/ml CP and PQ, and mitochondrial superoxide was measured by staining with the fluorescent dye MitoSOX and MitoTracker Red CM-H₂XRos. (a) The amount of mitochondrial superoxide production was visually confirmed by fluorescence microscopy. Scale bars, 100 μm. (b) The total amount of fluorescently stained by MitoSOX was quantified by FACS analysis (). (c) MitoTracker Red CM-H₂XRos intensity was quantified by microplate fluorometer (). (d–f) SN4741 cells were treated with 10 μg/ml CP and 400 μM PQ for 24 h. (d) Western blotting revealed the expression of MnSOD and Cu/ZnSOD proteins, which can remove superoxide (). MnSOD: mitochondrial SOD; Cu/ZnSOD: cytosolic SOD. (e) Quantification of mitochondrial SOD (). (f) Quantification of cytosolic SOD (). (g) CP potentiated the dopaminergic neuron-killing effect of H₂O₂, an exogenous ROS, in SN4741 cells (). (h) The rate of PQ recycling, a key step in the production of ROS by PQ, was confirmed by enzymatic assay using mitochondria isolated from the SN4741 cell line (). All data are representative of three independent experiments. ; by 2-tailed unpaired Student’s -test in (c, h) and by one-way ANOVA in (e–g); ns: not significant. Error bars represent +SD.

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