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Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Sulfur Assimilation01:20

Sulfur Assimilation

Sulfur is an essential element in biological systems, contributing to synthesizing key biomolecules, including amino acids such as cysteine and methionine, and cofactors such as coenzyme A and biotin. Microorganisms primarily assimilate sulfur as sulfate (SO₄²⁻) from the environment, which must undergo a series of biochemical transformations before it can be incorporated into cellular components. As sulfate is highly oxidized, it must undergo assimilatory sulfate reduction to become...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

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Related Experiment Video

Updated: Jun 4, 2026

Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
12:15

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

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Preventing metal-mediated oxidative DNA damage with selenium compounds.

Erin E Battin1, Matthew T Zimmerman, Ria R Ramoutar

  • 1Clemson University, South Carolina, USA.

Metallomics : Integrated Biometal Science
|February 3, 2011
PubMed
Summary

Selenium compounds inhibit metal-induced DNA damage by binding to copper and iron. This metal binding is crucial for their antioxidant activity, though not sufficient on its own.

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Last Updated: Jun 4, 2026

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

  • Biochemistry
  • Toxicology
  • Medicinal Chemistry

Background:

  • Transition metals like copper and iron generate hydroxyl radicals (˙OH), contributing to oxidative damage and disease.
  • Antioxidants can mitigate metal-induced DNA damage, highlighting potential therapeutic strategies.

Purpose of the Study:

  • To evaluate the efficacy of ten selenium compounds in preventing metal-mediated DNA damage.
  • To elucidate the mechanism underlying the antioxidant activity of selenium compounds in relation to metal ions.

Main Methods:

  • DNA gel electrophoresis assays were employed to quantify inhibition of hydroxyl radical-induced DNA damage.
  • Mass spectrometry was used to determine the stoichiometry of metal-selenium compound complexes.
  • Electrochemical analysis and glutathione peroxidase activity assays were performed.

Main Results:

  • Selenocystine, selenomethionine, and methyl-selenocysteine demonstrated significant inhibition of Cu(I)/H(2)O(2)-mediated DNA damage (IC50 values 3.34–25.1 μM).
  • Four selenium compounds also protected DNA from Fe(II)/H(2)O(2)-induced damage.
  • Metal coordination, particularly a 1:1 stoichiometry, was identified as necessary but not sufficient for antioxidant activity.
  • Glutathione peroxidase activity did not correlate with DNA damage inhibition.

Conclusions:

  • Metal binding is a primary mechanism for the antioxidant activity of selenium compounds.
  • The chemical structure of the selenium compound and the specific metal ion influence antioxidant efficacy.
  • Selenium compounds' ability to inhibit metal-mediated DNA damage is linked to their metal-chelating properties.