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Related Concept Videos

Oxidation of Alcohols02:37

Oxidation of Alcohols

In this lesson, the oxidation of alcohols is discussed in depth. The various reagents used for oxidation of primary and secondary alcohols are detailed, and their mechanism of action is provided.
The process of oxidation in a chemical reaction is observed in any of the three forms:
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...
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.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

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).
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...
Radical Oxidation of Allylic and Benzylic Alcohols01:21

Radical Oxidation of Allylic and Benzylic Alcohols

Activated manganese(IV) oxide can selectively oxidize allylic and benzylic alcohols via a radical intermediate mechanism. Primary allylic alcohols are oxidized to aldehydes, while secondary allylic alcohols yield ketones. The redox reaction of potassium permanganate with an Mn(II) salt such as manganese sulfate (under either alkaline or acidic conditions), followed by thorough drying, yields the oxidizing agent: activated MnO2. While MnO2 is insoluble in the solvents used for the reaction, the...

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Related Experiment Video

Updated: May 30, 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

Published on: May 29, 2019

Alcohol consumption and oxidative DNA damage.

Takeshi Hirano1

  • 1Department of Life and Environment Engineering, Faculty of Environmental Engineering, The University of Kitakyushu, 1-1 Hibikino, Wakamatsu-ku, Kitakyushu, Fukuoka 808-0135, Japan. t-hirano@env.kitakyu-u.ac.jp

International Journal of Environmental Research and Public Health
|August 17, 2011
PubMed
Summary

High alcohol consumption and poor diet elevate cancer risk by increasing DNA damage (8-oxo-Gua). Low alcohol intake may reduce this risk, highlighting concentration and diet as key factors in alcohol-related cancer.

Keywords:
7,8-dihydro-8-oxoguanine8-oxoguanine DNA glycosylase 1alcoholreactive oxygen speciesvitamin-depleted diet

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HPLC Measurement of the DNA Oxidation Biomarker, 8-oxo-7,8-dihydro-2’-deoxyguanosine, in Cultured Cells and Animal Tissues
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Comet Assay as an Indirect Measure of Systemic Oxidative Stress
08:23

Comet Assay as an Indirect Measure of Systemic Oxidative Stress

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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
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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HPLC Measurement of the DNA Oxidation Biomarker, 8-oxo-7,8-dihydro-2’-deoxyguanosine, in Cultured Cells and Animal Tissues
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HPLC Measurement of the DNA Oxidation Biomarker, 8-oxo-7,8-dihydro-2’-deoxyguanosine, in Cultured Cells and Animal Tissues

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Comet Assay as an Indirect Measure of Systemic Oxidative Stress
08:23

Comet Assay as an Indirect Measure of Systemic Oxidative Stress

Published on: May 22, 2015

Area of Science:

  • Biochemistry
  • Toxicology
  • Oncology

Background:

  • Alcohol consumption is a known risk factor for various cancers.
  • Oxidative DNA damage, specifically 8-oxo-guanine (8-oxo-Gua), is implicated in carcinogenesis.
  • The interplay between ethanol intake, diet, and DNA damage requires further investigation.

Purpose of the Study:

  • To investigate the impact of ethanol consumption on oxidative DNA damage and repair in rat liver and esophagus.
  • To determine how different ethanol concentrations and dietary patterns influence 8-oxo-Gua levels and repair activity.

Main Methods:

  • Utilized a previously established protocol for feeding rats high concentrations of ethanol.
  • Measured 8-oxo-Gua generation and repair activity in liver and esophageal tissues.
  • Examined effects of low ethanol concentration in mice treated with a carcinogen.

Main Results:

  • High ethanol concentration combined with a vitamin-depleted diet significantly increased 8-oxo-Gua generation and repair activity.
  • Increased 8-oxo-Gua is linked to point mutations and potential carcinogenesis.
  • Low ethanol concentration decreased 8-oxo-Gua and its repair activity in carcinogen-treated mouse livers.

Conclusions:

  • High ethanol intake and irregular diets increase the risk of liver and esophageal cancer.
  • Ethanol's effect on cancer risk is concentration-dependent.
  • Dietary patterns play a crucial role in modulating ethanol's impact on DNA damage and cancer risk.