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. Author manuscript; available in PMC: 2012 Jan 1.
Published in final edited form as: J Pineal Res. 2010 Oct 20;50(1):78–82. doi: 10.1111/j.1600-079X.2010.00815.x

Fig. 2.

Fig. 2

Melatonin-induced ROS generation in kidney mitochondria and the effects of mitochondrial blockers. Mitochondria were prepared from mouse kidney and labeled with DCF (1 µM) and ROS generation was indexed by the changes in DCF fluorescence. The traces in (A) represented the ROS generation in response to different concentrations of melatonin; the rate of melatonin-induced ROS formation increased with increasing melatonin concentration (B). Traces in (C) showed the effect of pretreatment of isolated kidney mitochondria with vehicle (control), the mitochondrial complex I inhibitor rotenone (5 µM), the mitochondrial complex III blockers myxothiazol (5 µM) or antimycin A (5 µM) on melatonin-induced ROS generation. Traces in (D) showed that addition of antimycin A (5 µM) after the start of melatonin-induced ROS production halted completely further ROS generations. The values in (E) were mean±SE rate of melatonin-induced ROS generation in mitochondria treated with vehicle (control), rotenone, antimycin A and myxothiazol from 3–5 experiments.