Vol. 272, No. 32, Issue of August 8, 1997 | Kenneth B. Beckman and Bruce N. Ames
The study of DNA oxidation has evolved from an exploratory phase to a field with numerous applications. Early research focused on the characterization of radiation-induced oxidative DNA lesions and their connection to cancer, leading to increased interest in DNA oxidation and potential damage from biological oxidants. Various techniques have been developed to measure oxidative DNA damage, including gas chromatography-mass spectrometry (GC-MS) and high-performance liquid chromatography-electrochemical detection (HPLC-EC). Despite methodological challenges, recent studies have shown growing congruence between different approaches.
The mechanisms and locations of DNA oxidation are complex, involving superoxide anion radicals, iron, and hydrogen peroxide. Reactive nitrogen intermediates and peroxidation of membrane lipids also contribute to DNA damage. DNA repair pathways, such as the "GO system" in E. coli, play a crucial role in removing oxidative lesions, and their dysfunction can lead to increased mutagenesis.
Oxidative DNA damage is a significant contributor to human cancer, influenced by factors like smoking, chronic inflammation, and endogenous oxidants. Epidemiological evidence suggests that antioxidants can reduce cancer risk. The role of DNA oxidation in aging and developmental abnormalities is less well-established but is an area of active research.
Recent studies have highlighted the importance of oxidative damage in various diseases and the potential for antioxidants to mitigate this damage. Transgenic mouse models are being used to further investigate the impact of oxidative stress on mutagenesis and cancer.The study of DNA oxidation has evolved from an exploratory phase to a field with numerous applications. Early research focused on the characterization of radiation-induced oxidative DNA lesions and their connection to cancer, leading to increased interest in DNA oxidation and potential damage from biological oxidants. Various techniques have been developed to measure oxidative DNA damage, including gas chromatography-mass spectrometry (GC-MS) and high-performance liquid chromatography-electrochemical detection (HPLC-EC). Despite methodological challenges, recent studies have shown growing congruence between different approaches.
The mechanisms and locations of DNA oxidation are complex, involving superoxide anion radicals, iron, and hydrogen peroxide. Reactive nitrogen intermediates and peroxidation of membrane lipids also contribute to DNA damage. DNA repair pathways, such as the "GO system" in E. coli, play a crucial role in removing oxidative lesions, and their dysfunction can lead to increased mutagenesis.
Oxidative DNA damage is a significant contributor to human cancer, influenced by factors like smoking, chronic inflammation, and endogenous oxidants. Epidemiological evidence suggests that antioxidants can reduce cancer risk. The role of DNA oxidation in aging and developmental abnormalities is less well-established but is an area of active research.
Recent studies have highlighted the importance of oxidative damage in various diseases and the potential for antioxidants to mitigate this damage. Transgenic mouse models are being used to further investigate the impact of oxidative stress on mutagenesis and cancer.