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Arthur I. Cederbaum
Researcher at Icahn School of Medicine at Mount Sinai
Publications - 375
Citations - 27906
Arthur I. Cederbaum is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Oxidative stress & Lipid peroxidation. The author has an hindex of 73, co-authored 375 publications receiving 26362 citations. Previous affiliations of Arthur I. Cederbaum include City University of New York & Rutgers University.
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Antioxidant properties of S-adenosyl-l-methionine in Fe2+-initiated oxidations
TL;DR: Results suggest that SAM inhibits alcohol and lipid oxidation mainly by Fe2- chelation and inhibition of Fe2+ autoxidation, which could represent an important mechanism by which SAM exerts cellular protective actions and reduces oxidative stress in biological systems.
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Increased oxygen radical-dependent inactivation of metabolic enzymes by liver microsomes after chronic ethanol consumption.
Elisa Dicker,Arthur I. Cederbaum +1 more
TL;DR: The enhanced generation of reactive oxygen intermediates and increased inactivation of enzymes by microsomes may contribute toward the hepatotoxic effects associated with ethanol consumption.
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Rapid decrease of cytochrome P-450IIE1 in primary hepatocyte culture and its maintenance by added 4-methylpyrazole.
TL;DR: The results suggest that the already induced P‐ 450IIE1 isozyme is more labile and subject to rapid decline in culture and that inducers such as 4‐methylpyrazole appear to stabilize the P‐450IIE 1 and thus help to maintain this isozyme and associated catalytic activity in cultures prepared from noninduced and induced hepatocytes.
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Overexpression of Catalase in the Mitochondrial or Cytosolic Compartment Increases Sensitivity of HepG2 Cells to Tumor Necrosis Factor-α-induced Apoptosis
TL;DR: Results suggest that catalase, overexpressed in the cytosolic or especially the mitochondrial compartment, potentiates TNF-α-induced apoptosis and activation of caspases by removal of H2O2.
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Increased Cytotoxicity of 3-Morpholinosydnonimine to HepG2 Cells in the Presence of Superoxide Dismutase ROLE OF HYDROGEN PEROXIDE AND IRON
TL;DR: The results suggest that the potentiation of SIN-1 toxicity by SOD is due to enhanced production of H2O2, followed by site-specific damage of critical cellular sites by a transition metal-catalyzed reaction.