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Related Concept Videos

Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Nucleotide Excision Repair01:38

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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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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...
Base Excision Repair01:54

Base Excision Repair

One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Mutations01:35

Mutations

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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DNA damage after long-term repetitive hyperbaric oxygen exposure.

Michael Gröger1, Sükrü Oter, Vladislava Simkova

  • 1Sektion Anästhesiologische Pathopyhsiologie und Verfahrensentwicklung Universitätsklinikum, Parkstrasse 11, D-89073 Ulm, Germany.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|November 22, 2008
PubMed
Summary

Long-term hyperbaric oxygen (HBO) exposure did not alter baseline DNA damage or antioxidant capacity in combat divers. However, their lymphocytes showed increased susceptibility to oxidative DNA damage following ex vivo HBO exposure.

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Area of Science:

  • Biomedical Science
  • Physiology
  • Toxicology

Background:

  • Hyperbaric oxygen (HBO) therapy involves breathing pure oxygen at pressures above normal atmospheric levels.
  • Single HBO exposures induce oxidative DNA damage, but this is typically repaired with adaptive protection.
  • Repetitive HBO exposure, common in diving professions, may alter oxidative stress responses.

Purpose of the Study:

  • To investigate the effects of long-term, repetitive hyperbaric oxygen (HBO) exposure on DNA damage and oxidative stress.
  • To compare oxidative stress markers and DNA repair capacity in combat divers versus control groups.
  • To determine if chronic HBO exposure modifies susceptibility to oxidative DNA damage.

Main Methods:

  • Assessed in vivo DNA damage (comet assay), antioxidant enzyme activity, and glutathione status in combat swimmers, divers, and control groups.
  • Measured ex vivo DNA damage and superoxide anion radical production in lymphocytes after a single HBO exposure.
  • Compared oxidative stress parameters and DNA damage response across different exposure groups.

Main Results:

  • In vivo oxidative stress and antioxidant capacity were similar across all groups.
  • Ex vivo HBO exposure increased DNA damage and superoxide production in lymphocytes for all participants.
  • Lymphocytes from combat swimmers exhibited a significantly greater increase in DNA damage and superoxide production post-HBO exposure.
  • DNA damage was fully repaired within 1 hour in all groups.

Conclusions:

  • Long-term repetitive hyperbaric oxygen (HBO) exposure does not appear to alter basal antioxidant capacity or DNA strand breaks in healthy, endurance-trained individuals.
  • Combat swimmers and divers show enhanced ex vivo susceptibility to HBO-induced oxidative DNA damage in their lymphocytes.
  • This enhanced susceptibility may indicate a specific adaptation or increased vulnerability to oxidative stress from repeated HBO exposure.