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Related Concept Videos

Chronic Pancreatitis I: Introduction01:25

Chronic Pancreatitis I: Introduction

Chronic pancreatitis is a long-standing, relapsing inflammation of the pancreas, characterized by irreversible damage to the gland. It results in progressive destruction of the pancreatic parenchyma, fibrosis, and eventual loss of both exocrine and endocrine function. The disease may evolve gradually after multiple episodes of acute pancreatitis or develop independently.EtiologyChronic pancreatitis can arise from a variety of causes:Alcohol use is the leading cause, accounting for 70–80% of...
Chronic Pancreatitis I: Introduction01:24

Chronic Pancreatitis I: Introduction

The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
Bioactivation and Tissue Toxicity01:25

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...
Phase I Oxidative Reactions: Overview01:19

Phase I Oxidative Reactions: Overview

Phase I biotransformation, or functionalization, is a crucial chemical process that converts drugs and other xenobiotics into more water-soluble forms, facilitating expulsion from the body. It involves oxidative, reductive, and hydrolytic reactions that add or unveil polar functional groups on lipophilic substrates. Key players in phase I reactions are the mixed-function oxidases. Situated in liver cell microsomes, these enzymes predominantly carry out drug metabolism. They require molecular...
Phase I Reactions: Oxidation of Aliphatic and Aromatic Carbon-Containing Systems01:19

Phase I Reactions: Oxidation of Aliphatic and Aromatic Carbon-Containing Systems

Phase I biotransformation reactions are integral to drug metabolism, predominantly involving oxidative, reductive, and hydrolytic transformations. Chief among these are oxidative reactions, which enhance the hydrophilicity of xenobiotics and introduce polar functional groups to facilitate their elimination from the body.
Oxidation reactions are fundamental in aromatic carbon-containing systems. An example is the hydroxylation of phenobarbital, a process that transforms it into...

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Related Experiment Video

Updated: Jun 13, 2026

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer
08:37

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

Published on: November 15, 2024

Chronic alcohol exposure increases circulating bioactive oxidized phospholipids.

Lili Yang1, Calivarathan Latchoumycandane, Megan R McMullen

  • 1Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio 44195, USA.

The Journal of Biological Chemistry
|May 13, 2010
PubMed
Summary

Ethanol metabolism causes liver damage and releases oxidized lipids into circulation, signaling alcoholic liver disease progression. Taurine supplementation reduced liver injury and these circulating lipid markers.

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Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder
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Related Experiment Videos

Last Updated: Jun 13, 2026

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer
08:37

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

Published on: November 15, 2024

Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder
05:12

Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder

Published on: June 23, 2023

Area of Science:

  • Hepatology
  • Toxicology
  • Lipidomics

Background:

  • Ethanol metabolism in the liver generates reactive oxygen species, causing oxidative stress and damage.
  • The mechanisms by which liver damage affects distal organs are not fully understood.
  • Oxidized lipids may mediate the systemic effects of liver injury.

Purpose of the Study:

  • To investigate the role of circulating oxidized lipids in alcoholic liver disease.
  • To identify specific oxidized lipids released into circulation during chronic ethanol ingestion.
  • To determine the relationship between liver damage, oxidative stress, and circulating oxidized lipids.

Main Methods:

  • Analysis of rat plasma using tandem mass spectrometry after chronic ethanol feeding.
  • Analysis of human plasma from patients with alcoholic steatohepatitis.
  • Correlation analysis between lipid markers, ethanol exposure, liver enzymes, and inflammatory markers.

Main Results:

  • Elevated levels of peroxidized phosphatidylcholines, oxidatively truncated phospholipids, and platelet-activating factor in ethanol-fed rats and patients with steatohepatitis.
  • Circulating oxidized lipids did not directly correlate with hepatic oxidative stress or liver damage markers.
  • Taurine administration prevented liver damage and reduced circulating oxidized lipid levels.

Conclusions:

  • Circulating oxidized phospholipids are markers of alcoholic steatohepatitis, distinct from direct hepatic oxidative stress.
  • These lipids are pro-inflammatory and pro-apoptotic, potentially mediating systemic effects of chronic ethanol exposure.
  • Targeting hepatic inflammation, rather than ethanol metabolism, may reduce circulating inflammatory mediators.