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Related Concept Videos

Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Peroxisomes01:24

Peroxisomes

Peroxisomes are specialized organelles present in fungi, plant, and animal cells. It can vary in number, size, morphology, and activity depending on the type of tissue and the nutritional state of the cell. For example, cells with active lipid metabolism, such as adipocytes, neurons, and hepatocytes, have more peroxisomes than other cells in the body. Besides their primary role in breaking down complex organic molecules, peroxisomes can also synthesize specific macromolecules and participate in...
Peroxisomes01:24

Peroxisomes

Peroxisomes are specialized organelles present in fungi, plant, and animal cells. It can vary in number, size, morphology, and activity depending on the type of tissue and the nutritional state of the cell. For example, cells with active lipid metabolism, such as adipocytes, neurons, and hepatocytes, have more peroxisomes than other cells in the body. Besides their primary role in breaking down complex organic molecules, peroxisomes can also synthesize specific macromolecules and participate in...
Protein Import into the Peroxisomes01:27

Protein Import into the Peroxisomes

Cells contain membrane-bound organelles called peroxisomes that oxidize organic molecules by transferring hydrogen atoms to oxygen, producing hydrogen peroxide. Peroxisomes enzymatically convert the released hydrogen peroxide into water and oxygen.
Peroxisomal Protein Import:
Peroxisomes lack the genetic machinery required to code for their own proteins. Hence, most peroxisomal membrane, lumenal and transmembrane proteins are synthesized in the cytoplasm or ER and transported to the peroxisome...
Radical Autoxidation01:20

Radical Autoxidation

The oxidation of an organic compound in the presence of air or oxygen is called autoxidation. For example, cumene reacts with oxygen to form hydroperoxide. Autoxidation involves initiation, propagation, and termination steps. Many organic compounds are susceptible to autoxidation—especially ethers in the presence of oxygen, which form hydroperoxides. Even though this reaction is slow, old ether bottles contain small amounts of peroxide, which leads to laboratory explosions during ether...
Overview of Fatty Acid Metabolism01:28

Overview of Fatty Acid Metabolism

Lipids also are sources of energy that power cellular processes. Like carbohydrates, lipids are composed of carbon, hydrogen, and oxygen, but these atoms are arranged differently. Most lipids are nonpolar and hydrophobic. Major types include fats and oils, waxes, phospholipids, and steroids.
Fatty acids are catabolized in a process called beta-oxidation, which takes place in the matrix of the mitochondria and converts their fatty acid chains into two-carbon units of acetyl groups. The acetyl...

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The Relation of Autolysis to the Histological changes occurring in Necrotic Areas.

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Related Experiment Video

Updated: Jun 19, 2026

Measurement of Fatty Acid β-Oxidation in a Suspension of Freshly Isolated Mouse Hepatocytes
11:03

Measurement of Fatty Acid β-Oxidation in a Suspension of Freshly Isolated Mouse Hepatocytes

Published on: September 9, 2021

THE RELATION OF FATTY DEGENERATION TO THE OXIDATION OF PURINES BY LIVER CELLS.

H G Wells1

  • 1Department of Pathology, University of Chicago.

The Journal of Experimental Medicine
|October 30, 2009
PubMed
Summary

Fatty liver changes induced by hydrazine and phosphorus do not impair the liver's ability to oxidize uric acid or xanthine. This suggests fatty degeneration may not be incompatible with cellular metabolic activity.

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Determination of Fatty Acid Oxidation and Lipogenesis in Mouse Primary Hepatocytes
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Determination of Fatty Acid Oxidation and Lipogenesis in Mouse Primary Hepatocytes

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In Vitro Modeling of Fat Deposition in Metabolic Dysfunction-Associated Steatotic Liver Disease
07:03

In Vitro Modeling of Fat Deposition in Metabolic Dysfunction-Associated Steatotic Liver Disease

Published on: July 19, 2024

Related Experiment Videos

Last Updated: Jun 19, 2026

Measurement of Fatty Acid β-Oxidation in a Suspension of Freshly Isolated Mouse Hepatocytes
11:03

Measurement of Fatty Acid β-Oxidation in a Suspension of Freshly Isolated Mouse Hepatocytes

Published on: September 9, 2021

Determination of Fatty Acid Oxidation and Lipogenesis in Mouse Primary Hepatocytes
12:11

Determination of Fatty Acid Oxidation and Lipogenesis in Mouse Primary Hepatocytes

Published on: August 27, 2015

In Vitro Modeling of Fat Deposition in Metabolic Dysfunction-Associated Steatotic Liver Disease
07:03

In Vitro Modeling of Fat Deposition in Metabolic Dysfunction-Associated Steatotic Liver Disease

Published on: July 19, 2024

Area of Science:

  • Biochemistry
  • Cell Biology
  • Toxicology

Background:

  • Fatty liver (steatosis) is a condition characterized by the accumulation of fat in liver cells.
  • The impact of severe fatty degeneration on cellular enzyme function, particularly those involved in oxidation, is not fully understood.
  • Uricolytic and xanthine oxidase enzymes are considered late-developing and potentially vulnerable to cellular injury.

Purpose of the Study:

  • To investigate the effect of chemically induced severe fatty liver on the oxidative capacity of liver enzymes in vitro.
  • To determine if extreme fatty metamorphosis compromises the function of uricolytic and xanthine oxidase enzymes.
  • To assess the general compatibility of fatty degeneration with hepatic metabolic activity.

Main Methods:

  • Induction of severe fatty liver in experimental models using hydrazine and phosphorus.
  • In vitro assessment of liver tissue's capacity to oxidize uric acid and xanthine.
  • Comparison of enzyme activity in fatty liver tissue versus normal liver tissue.

Main Results:

  • High degrees of fatty change in the liver were achieved with minimal necrosis.
  • Liver tissue with extreme fatty metamorphosis retained its ability to oxidize uric acid and xanthine in vitro.
  • The uricolytic enzyme and xanthine oxidase activity were not significantly diminished despite severe steatosis.

Conclusions:

  • Extreme fatty metamorphosis of hepatic cells does not destroy or significantly impair the uricolytic and xanthine oxidase enzymes.
  • Fatty degeneration may not be fundamentally incompatible with high cellular metabolic activity.
  • While direct enzyme injury seems minimal, secondary functional decreases in vivo are possible due to physical changes like capillary compression.