Fig. 2

In ovo injected BHP induced hepatic mitochondrial dysfunction and redox imbalance in embryo. The control and BHP groups were treated with either pbs or 600 μmol/L BHP by in ovo injection. A Hepatic ATP content. B Hepatic mtDNA copy number. C Representative electron microscopy micrographs of mitochondrial ultrastructure. The mitochondria from the BHP treated embryo was smaller with a condensed mitochondrial membrane density (red arrows). D–G The abundance heatmap of metabolites for energy metabolism by targeted metabolomic analysis (D) The relative abundance of metabolites related to TCA (E) and oxidative phosphorylation (E) and glycolysis (F). H Hepatic gene mRNA expression of CPT1, CPT2, VDAC, and TFAM related to mitochondrial function. I–J Hepatic GSH and MT4 contents in mitochondria. K Hepatic mRNA expression of MT1, MT4, Gpx, and SOD1 related to the antioxidant ability. L–M Representative band of hepatic MT4, Nrf-2, PGC-1α, and PPAR-α protein expression by Western blot assay. The data were analyzed using unpaired two-tailed Student's t-test (^∗P < 0.05). Data are mean ± SEM (n = 4–6)