Caspase-12 mediates carbon tetrachloride-induced hepatocyte apoptosis in mice

Figure 1 Dose- and time-dependent liver damage, apoptosis and reactive oxygen species generation. A: Carbon tetrachloride (CCl₄)-induced hepatic injury as measured by alanine aminotransferase (ALT) levels. Values are mean ± SE, n = 5, ^aP < 0.05 vs control, ^cP < 0.05 vs 12 h at the same dose; B: Hepatic apoptosis was examined by terminal transferase-mediated dUTP nick-end labeling (TUNEL) staining. For each sample, five randomly selected fields at 200× magnification were evaluated. Values are mean ± SE, n = 5; ^eP < 0.05 vs 100 μL/kg body weight group at the same time point; C: Generation of reactive oxygen species as measured by malondialdehyde (MDA) in both caspase-12^+/+ and -12^-/- mouse livers 12, 24 and 48 h following CCl₄ treatment (300 μL/kg body weight). Values are mean ± SE, n = 8; ^gP < 0.05 vs controls.