Superoxide dismutase ameliorates oxidative stress and regulates liver transcriptomics to provide therapeutic benefits in hepatic inflammation
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Background Oxidative stress refers to the imbalance between oxidants and antioxidants in organisms and often induces hepatic inflammation. Supplementing exogenous superoxide dismutase is an effective way to alleviate oxidative stress; however, the effects and mechanisms by which superoxide dismutase alleviates hepatic inflammation remain unclear. Methods This study established a Kunming mouse model to verify and investigate the oxidative stress and hepatic inflammation-alleviating effects of the superoxide dismutase oral supplement that was prepared by our research group in a previous study. Results The superoxide dismutase product significantly restored the body weight and liver alanine transaminase, aspartate aminotransferase, superoxide dismutase, catalase, glutathione, and glutathione peroxidase levels of oxidative stress induced mice. Moreover, exogenous superoxide dismutase significantly inhibited interleukin 1 β and interleukin 6 mRNA expression in the livers of mice with hepatic inflammation. Transcriptomic analysis indicated that superoxide dismutase had a significant inhibitory effect on Endog expression, alleviating oxidative stress damage, and mediating liver cell apoptosis by regulating the expression of Rab5if , Hnrnpab , and Ifit1 . Conclusion Our research verified the oxidative stress remediation effects of superoxide dismutase and its therapeutic role against hepatic inflammation. This study can lay a foundation for investigating the mechanism by which superoxide dismutase alleviates hepatic disease.Reactive nitrogen species
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It is well established that the accumulation of high levels of reactive oxygen species (ROS), due to excessive generation of ROS and/or impaired antioxidant capacity of cells, can result in oxidative stress and cause oxidative damage to cells and their functions [...]
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Oxygen toxicity
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Some commercial samples of bovine catalase contain superoxide dismutase activity. Therefore the inhibition of a reaction on the addition of a catalase preparation need not necessarily mean that H2O2 is responsible for the reaction.
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Myocardial damage during ischaemia-reperfusion is partly mediated by the accelerated production of reactive oxygen species (ROS). Under physiological conditions, antioxidants, such as catalase, regulate ROS levels. The capacity for elevated catalase levels to offer cardio-protective benefits to hearts exposed to ischaemia-reperfusion has been demonstrated previously. However, no studies thus far have selectively inhibited catalase in isolated cardiomyocytes, This study investigated the importance of endogenous catalase in regulating ROS generation basally and during oxidative stress by using the catalase inhibitor, 3-amino-1,2,4-triazole (3-AT). Cardiomyocytes were isolated from adult rat hearts. Cells were loaded with 5-(and-6)-chloromethyl-2’,7’-dichlorodihydrofluorescein diacetate acetyl ester (CM-H2DCFDA) in the presence or absence of different concentrations of 3-AT (0–40 mM). The ROS production rate in quiescent cardiomyocytes was estimated by measuring the fluorescence signal emitted by 5-(and 6)-chloromethyl-2′,7′-dichlorofluorescein, using a fluorescence plate reader. Incubation with 3-AT did not affect the ROS generation rate under basal conditions. However, upon addition of 10 mM H2O2, 3-AT administration resulted in a dose-dependent increase in the ROS generation rate (P < 0.0001). This increase plateaued with 20 mM 3-AT, which resulted in a near-tripling of the mean ROS generation rate compared to 0 mM 3-AT (P < 0.01). This study demonstrates that endogenous catalase has a limited contribution to the regulation of ROS levels in resting, unstressed cardiomyocytes. However, its activity appears important in reducing the ROS generation rate when intracellular H2O2 levels are elevated. We conclude that, despite the low levels of endogenous catalase present in cardiomyocytes, its regulation of ROS generation is very important during conditions of significant oxidative stress.
Dichlorofluorescein
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Dismutase
White (mutation)
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Mitochondria are known to generate approximately 90% of cellular reactive oxygen species (ROS). The imbalance between mitochondrial reactive oxygen species (mtROS) production and removal due to overproduction of ROS and/or decreased antioxidants defense activity results in oxidative stress (OS), which leads to oxidative damage that affects several cellular components such as lipids, DNA, and proteins. Since the kidney is a highly energetic organ, it is more vulnerable to damage caused by OS and thus its contribution to the development and progression of chronic kidney disease (CKD). This article aims to review the contribution of mtROS and OS to CKD progression and kidney function deterioration.
Mitochondrial ROS
Overproduction
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