Physiological concentrations of unconjugated bilirubin (UCB) prevent hepatocellular oxidative injury

BASIGLIO CL; TOLEDO FD; ARRIAGA SM; SANCHEZ POZZI EJ; MOTTINO AD; ROMA MG

San Pedro

Congreso; VII Meeting of the SFRBM - South American Group; 2011

Society for Free Radical Biology and Medicine (SFRBM)

Our group showed that oxidative stress induces cholestasis by triggering actin disarrangement and further endocytic internalization of canalicular transporters of bile salts (Bsep) and glutathione (Mrp2) (FRBM 40: 2005, 2006; Toxicol Sci. 91: 150, 2006). Bilirubin is an endogenous antioxidant, although its protective role in hepatopathies is uncertain. Here, we evaluated the capacity of UCB to limit hepatocellular oxidative injury and alterations in localization/function of canalicular transporters, using the model pro-oxidant agent tert-butilhydroperoxide (tBOOH). Physiological concentrations of UCB (1.7?17.1 µM) prevented by 40 % tBOOH (500 µM)-induced membrane lipid peroxidation (assessed by the TBARS method), in isolated rat hepatocytes (p