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Hence, hepatocytes are equipped with abundant antioxidant enzymes to counterbalance this oxidative challenge.16 However, this borderline equilibrium makes liver highly susceptible to the pro-oxidant injury induced by pathological conditions that disrupt this balance, by enhancing ROS formation, by impairing the antioxidant defences, or both.17-19 Indeed, oxidative stress is a common feature in most hepatopathies including hepatic ischemia-reperfusion injury following hepatectomy or liver transplantation,20,21 obstructive cholestasis,22 chronic cholestatic liver diseases,23-27 sepsis-induced cholestasis,28 viral,29,30 toxic31 and autoimmune32 hepatitis, alcoholic30,33 and non-alcoholic34-36 steatohepatitis, and pathologies leading to hepatic accumulation of metals, such as iron (hemochromatosis, iron-loading anaemia)37,38 or copper (Wilsons disease).39 Much attention has been focused on the mechanism of oxidative-stress-induced hepatocellular death.40-43 However, this usually involves only a limited number of hepatocytes

Nitric oxide acts as an antioxidant and delays programmed cell death in barley aleurone layers

Phase II studies, including those on radiation-induced hemorrhagic cystitis, further investigate the safety of sodium copper chlorophyllin at a daily dose of 750 mg (Krishnatry et al

Vascular superoxide production by NAD(P)H oxidase: association with endothelial dysfunction and clinical risk factors

O.LemmersH.Toenhake-DijkstraH.FossatiG.JansenT

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