Related Experiment Video

Updated: Aug 30, 2026

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Chromosomal DNA fragmentation in apoptosis and necrosis induced by oxidative stress

Yoshihiro Higuchi1

  • 1Department of Molecular Pharmacology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8640, Japan. higuchiy@med.kanazawa-u.ac.jp

Biochemical Pharmacology
|October 14, 2003
PubMed

Insights

Oxidative stress causes DNA fragmentation in mammalian cells, leading to cell death via apoptosis or necrosis. This process involves reactive oxygen species (ROS) and is influenced by factors like polyunsaturated fatty acids.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Chromosomal DNA dysfunction is implicated in mammalian cell death.
  • Oxidative stress generates reactive oxygen species (ROS), inducing DNA fragmentation and cell demise.
  • DNA fragmentation can occur through apoptosis or necrosis pathways.

Purpose of the Study:

  • To investigate the mechanisms of ROS-mediated DNA fragmentation in mammalian cells.
  • To classify nucleases involved in chromosomal DNA fragmentation during cell death.
  • To explore the role of polyunsaturated fatty acids (PUFAs) and glutathione (GSH) in oxidative stress-induced DNA damage.

Main Methods:

  • Analysis of DNA fragmentation patterns (giant DNA, HMW DNA, internucleosomal fragments) induced by oxidative stress.
  • Investigation of the role of lipid peroxidation and PUFAs in ROS-mediated DNA damage.
  • Assessment of cell death pathways (apoptosis vs. necrosis) under conditions of altered intracellular GSH levels and ROS accumulation.

Main Results:

  • Oxidative stress induces significant chromosomal DNA fragmentation, producing various DNA fragment sizes.
  • Polyunsaturated fatty acids (PUFAs) and their hydroperoxides enhance ROS-mediated DNA fragmentation via lipid peroxidation.
  • Reduced intracellular GSH levels lead to ROS overproduction and accumulation, triggering cell death.

Conclusions:

  • ROS-mediated DNA fragmentation is a key event in oxidative stress-induced mammalian cell death.
  • The interplay between ROS, lipid peroxidation, and GSH levels significantly influences cell fate.
  • Understanding these mechanisms is crucial for differentiating between apoptosis and necrosis in response to oxidative damage.

More Related Videos

Quantifying the Level of 8-oxo-dG Using ELISA Assay to Evaluate Oxidative DNA Damage in MCF-7 Cells05:13

Quantifying the Level of 8-oxo-dG Using ELISA Assay to Evaluate Oxidative DNA Damage in MCF-7 Cells

Published on: May 24, 2024

Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter12:15

Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter

Published on: May 29, 2019

Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...