Abstract
Oxidative stress induced by the overproduction of free radicals or reactive oxygen species (ROS) has been considered as a key pathogenic mechanism contributing to the initiation and progression of injury in liver diseases. Consequently, during the last few years antioxidant substances, such as superoxide dismutase (SOD), resveratrol, colchicine, eugenol, and vitamins E and C have received increasing interest as potential therapeutic agents in chronic liver diseases. These substances have demonstrated their efficacy in equilibrating hepatic ROS metabolism and thereby improving liver functionality. However, many of these agents have not successfully passed the scrutiny of clinical trials for the prevention and treatment of various diseases, mainly due to their unspecificity and consequent uncontrolled side effects, since a minimal level of ROS is needed for normal functioning. Recently, cerium oxide nanoparticles (CeO2NPs) have emerged as a new powerful antioxidant agent with therapeutic properties in experimental liver disease. CeO2NPs have been reported to act as a ROS and reactive nitrogen species (RNS) scavenger and to have multi-enzyme mimetic activity, including SOD activity (deprotionation of superoxide anion into oxygen and hydrogen peroxide), catalase activity (conversion of hydrogen peroxide into oxygen and water), and peroxidase activity (reducing hydrogen peroxide into hydroxyl radicals). Consequently, the beneficial effects of CeO2NPs treatment have been reported in many different medical fields other than hepatology, including neurology, ophthalmology, cardiology, and oncology. Unlike other antioxidants, CeO2NPs are only active at pathogenic levels of ROS, being inert and innocuous in healthy cells. In the current article, we review the potential of CeO2NPs in several experimental models of liver disease and their safety as a therapeutic agent in humans as well.
Highlights
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It is worth noting that thanks to this auto-regenerative redox cycle, CeO2 NPs can participate in these enzymatic reactions by catalytically degrading the excess of different reactive oxygen species (ROS)—i.e., without being totally consumed in the reaction and enabling longer and sustained activity compared with the shorter half-life of classic antioxidants
Two main histological categories may be considered in metabolic dysfunction-associated fatty liver disease (MAFLD): simple fatty liver, with a favorable clinical outcome, and non-alcoholic steatohepatitis (NASH), characterized by inflammation in addition to the fat infiltration of the liver, and at higher risk of developing fibrosis, cirrhosis, liver failure, and hepatocarcinoma
Summary
It is worth noting that thanks to this auto-regenerative redox cycle, CeO2 NPs can participate in these enzymatic reactions by catalytically degrading the excess of different ROS—i.e., without being totally consumed in the reaction and enabling longer and sustained activity compared with the shorter half-life of classic (small molecule) antioxidants. When doing this, due to their peculiar electronic structure, CeO2 NPs act as a buffer, balancing redox homeostasis This means that their biological activity is only carried out in the case of ROS overproduction [31] and they become a rather inert material in healthy physiological conditions, slowly dissolving into innocuous cerium ions which are expulsed via the urinary track or the hepatic route [32,33]. Even at low doses, they can be more effective and have long-lasting activity in a multiplicity of cross reactions between ROS and inflammation at any level, which will allow disconnecting these two events [15]
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