5′-Adenosine monophosphate–activated kinase phosphorylation during toxicity. (A) Cellular signaling schematic representation illustrating the convergence of protein kinase B (Akt) and 5′-adenosine monophosphate–activated kinases (AMPK) signaling on the mammalian target of rapamycin complex 1 (mTOR1), which controls downstream targets including p70 s6 kinase (p70s6k). (B) Western blots of cardiac lysates at different time points during recovery for the AMPK pathway including acetyl-CoA carboxylase (ACC) phosphorylated at S79; tuberous sclerosis 2 (TSC2) phosphorylated at S1387; AMPK phosphorylated at T172; and total AMPK and total glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as loading control. (C) Densitometry of phospho-AMPK and phospho-ACC comparing concentrations at baseline (n = 4) with concentrations during toxicity (n = 6); ****P < 0.0001, post hoc Sidak test. (D) Densitometry of phospho-TSC2 comparing concentrations at baseline (n = 4) with concentrations during toxicity (n = 6); *P < 0.0001, Sidak post hoc test.