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. 2011 Apr;162(8):1716–1730. doi: 10.1111/j.1476-5381.2010.01189.x

Figure 2.

Figure 2

Elimination of carboplatin (Cbpt)-mediated p47PHOX membrane translocation, NADPH oxidase activity, reactive oxygen species (ROS) production, and protein carbonyl group formation in renal tubular cells (RTC) overexpressing haem oxygenase (HO)-1. (A) RTC variants were challenged with 200 µM carboplatin for 1 h, and cell lysates were partitioned into membrane-cytosolic fractions for a Western blot analysis of activated p47PHOX. (B) NADPH oxidase in RTC variants challenged with 200 µM carboplatin for 1 h. Four samples were analysed in each group, and values are presented as the mean ± SEM of three independent experiments. *P < 0.05, significantly different from its respective cell variants alone; #P < 0.05, significantly different from RTC with additional carboplatin challenge. (C) ROS production in cell variants was subjected to 1 h of 200 µM carboplatin administration as previously described. (D) Cell variants were treated with 200 µM carboplatin for 24 h, and cell lysates were harvested and analysed for oxidative stress-mediated carbonyl formation by Western blotting. Representative CM-H2DCFDA fluorescent photomicrographs of carboplatin-mediated ROS production and Western blot analysis of carbonyl group formation induced by carboplatin in RTC variants with the above-mentioned treatments are shown. Ctrl, control.