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Related Concept Videos

Nucleotide Excision Repair01:38

Nucleotide Excision Repair

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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...
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Mutations01:35

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Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
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Overview of DNA Repair02:25

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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.
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Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).
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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...
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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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[How can an electron induce oxidative damage in DNA in solution].

Jun Ma1, Sergey Denisov2, Amitava Adhikary3

  • 1Professeur à l'Université de Nanjin en Chine (Aeronautics et Astronautics). Il a effectué sa thèse et une partie de son post-doctorat au Laboratoire de Chimie Physique.

L'Actualite Chimique
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Dissociative electron attachment (DEA) causes DNA damage in solution. Researchers found that quasi-free electrons, not presolvated ones, initiate damage by forming transient negative ions, leading to strand breaks via DEA.

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Area of Science:

  • Physical Chemistry
  • Radiation Chemistry
  • Biophysics

Context:

  • Dissociative electron attachment (DEA) is a known mechanism for DNA damage in gas and solid phases.
  • Understanding DEA-induced DNA damage in solution remains a significant challenge due to complex electron solvation dynamics.

Purpose:

  • To investigate the fundamental mechanisms of electron capture by DNA/RNA bases, nucleosides, and nucleotides in aqueous and diethylene glycol (DEG) solutions.
  • To elucidate the role of different electron states (quasi-free, presolvated, and solvated) in initiating DNA/RNA damage via DEA.

Summary:

  • Picosecond pulse radiolysis experiments revealed that quasi-free electrons (eqf-), not presolvated electrons (epre-), are primarily responsible for initiating DNA damage in aqueous solutions at low concentrations.
  • Contrary to existing hypotheses, presolvated electrons show limited capture of DNA/RNA components. However, a decrease in solvated electron yield and formation of nucleotide anion radicals confirm ultrafast electron-mediated DNA damage via DEA.
  • In DEG, quasi-free electrons effectively attach to ribothymidine, forming excited transient negative ions (TNI*) that dissociate the N1-C1' glycosidic bond, mimicking hydroxyl radical-induced damage.

Impact:

  • This study challenges previous assumptions about electron capture mechanisms in DNA/RNA damage, providing crucial insights into radiation-induced biological effects.
  • The findings highlight the distinct reactivity of different electron states in solution, crucial for understanding radiobiology and developing targeted radiation therapies.
  • Demonstrates that DEA can lead to DNA/RNA base damage and strand breaks, with implications for radiation protection and medical applications involving ionizing radiation.