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. 2011 Apr 20;301(1):F125–F133. doi: 10.1152/ajprenal.00041.2011

Fig. 1.

Fig. 1.

Chronic nicotine (NIC) exposure exacerbates injury of the kidney after acute ischemia-reperfusion (IR) and cultured proximal tubule cells after treatment with H2O2. A: expression of kidney injury molecule (KIM)-1 in kidney lysates from C57BL/6J mice that underwent renal IR injury was determined by Western blotting. One group received saccharine, while the other NIC as described in materials and methods. B: densitometry of results from A. Values are means ± SD of ratios of KIM-1/actin; n = 4 (sham) and n = 8 (IR). *P < 0.05 compared with sham. #P < 0.05 compared with saccharine group. @P < 0.05 compared with the saccharine group. C: TKPTS cells were pretreated or not with 200 μM NIC for 24 h before treatment with 200 μM H2O2. Lactate dehydrogenase (LDH) release was determined 24 h after treatment with H2O2. Values represent percentage of released LDH and expressed as means ± SD; n = 3. *P < 0.05 compared with untreated (none).

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