Hydrogen-rich water protects against acetaminophen-induced hepatotoxicity in mice

Figure 7 Schematic representation of the proposed effect of the hydrogen molecule in acetaminophen-induced hepatic injury. After acetaminophen (APAP) administration into the hepatocytes, APAP is first metabolized through the cytochrome P4502E (CYP2E1) and generates N-acetyl-p-benzoquinone imine (NAPQI), which binds with glutathione (GSH) and increases reactive oxygen species (ROS) and RNS formation as well as the level of inflammatory cytokines. It can also cause JNK phosphorylation that damages the mitochondria and endoplasmic reticulum. Meanwhile, connexin 32 (Cx32) can be induced with oxidative stress, which can promote the amplification of liver injury. The hepatic self-repair function is also activated after APAP administration, which can promote the cell mitosis to facilitate liver regeneration. In the present study, we found that hydrogen can reduce APAP hepatotoxicity by inhibiting APAP metabolism, ROS and RNS formation, Cx32 expression and promote hepatocyte proliferation.