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. Author manuscript; available in PMC: 2007 Oct 1.
Published in final edited form as: Am J Physiol Renal Physiol. 2006 May 16;291(4):F840–F855. doi: 10.1152/ajprenal.00219.2005

Fig. 10.

Fig. 10

Effect of TBHP-induced injury and inhibition of the MEK1/2-ERK1/2 pathway on the activities of pyruvate dehydrogenase (A), aconitase (B), α-ketoglutarate dehydrogenase (C), and malate dehydrogenase (D) in RPTC mitochondria at 4 h following the injury. RPTC were treated with TBHP (0.35 mM, 45 min), and samples were taken at 4 h of the recovery period to assess activities of pyruvate dehydrogenase, aconitase, α-ketoglutarate dehydrogenase, and malate dehydrogenase. Controls were treated with the diluent (DMSO, 0.01%). To inhibit ERK1/2 activation, some RPTC were treated with 10 μM U0126 before TBHP exposure and after each daily media change starting from the media change to remove TBHP. Mitochondria were isolated from RPTC at 4 h following TBHP-induced injury and enzymatic activities were determined spectrophotometrically as described in materials and methods. Results are average ± SE of 5 independent experiments (RPTC isolations). Values with dissimilar superscripts at a given time point are significantly different (P < 0.05) from each other.