Although the liver is the leading site for taurine (TAU) synthesis, the level
of this amino acid in hepatic tissue is relatively low. It is well-known that TAU is
efficiently redistributed from hepatocytes to the circulation. However, the human
body’s capacity for TAU synthesis is negligible, and we receive a very high percentage
of our body TAU from exogenous sources. Plasma TAU is taken up by several tissues,
such as the skeletal muscle and the heart. The roles of TAU in liver function are the
subject of many investigations. It has been found that TAU could have beneficial
effects against xenobiotics-induced liver injury, alcoholism-associated hepatic damage,
non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), or
even viral hepatitis infections. The inhibition of cytochrome P450, alleviation of
oxidative stress, inhibition of inflammatory reactions, and the mitigation of tissue
fibrosis are fundamental mechanisms proposed for the hepatoprotective properties of
TAU. On the other hand, many studies indicate that hepatocytes’ mitochondria are
essential targets for the cytoprotective properties of TAU. The current chapter reviews
the beneficial role of TAU on the most common liver disorders, focusing on the effects
of this amino acid on mitochondrial function and energy metabolism.
Keywords: Hepatoprotection, Hepatotoxicity, Liver disease, Liver injury, Mitochondria, Oxidative stress.
