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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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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Mechanisms of Hepatotoxicity

TL;DR: This review addresses recent advances in specific mechanisms of hepatotoxicity, including inducible nitric oxide synthase knockout mice, where nitration is prevented, but unscavenged superoxide production then causes toxic lipid peroxidation to occur instead.

Alcohol, oxidative stress, and free radical damage

TL;DR: ROS production and oxidative stress in liver cells play a central role in the development of alcoholic liver disease and alcohol reduces the levels of agents that can eliminate ROS (i.e., antioxidants).
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CYP2E1 and oxidative liver injury by alcohol.

TL;DR: This review article summarizes some of the biochemical and toxicological properties of CYP2E1 and briefly describes the use of cell lines developed to constitutively express CYP1-dependent and cytochrome P450 2E1 knockout mice in assessing the actions of CYE1.
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Role of oxidative stress in alcohol-induced liver injury

TL;DR: This review summarizes some of the leading pathways and discusses the evidence for their contribution to alcohol-induced liver injury, special emphasis is placed on CYP2E1, which is induced by alcohol and is reactive in metabolizing and activating many hepatotoxins, including ethanol, to reactive products, and in generating ROS.