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. 2024 May 8;73:103179. doi: 10.1016/j.redox.2024.103179

Fig. 5.

Fig. 5

Sirt3 knockout exacerbates Cd-induced mitochondrial GPX4 acetylation, renal cell ferroptosis and AKI. Wild type and Sirt3−/− male mice intraperitoneally injected with CdCl2 (4 mg/kg). Kidney tissues were collected 24 h after CdCl2. (A) SIRT3 was detected using immunoblot; (B) SIRT3/β-actin. (C–E) Mitochondrial GPX4 acetylation was analyzed by Co-IP. (C) Representative images. (D) Ace-Lysine binding efficiency. (E) GPX4/TOM20. (F–K) Targeted metabolomics of oxidized lipids were examined by LC-MS/MS. Renal oxidized metabolites of (F) A heatmap. (G)ARA, (H) LA, (I) ALA, (J) EPA and (K) DHA are shown. (L and M) Renal 4-HNE+ area was measured by IHC. (L) Representative images. (M) Quantitative analysis. (N and O) Renal pathology was evaluated. (N) Representative H&E images. (O) Pathological score. (P) Serum UA. All data are presented as mean ± S.E.M. (N = 6–8). *P < 0.05, **P < 0.01.