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Definition: How does oxidative stress impact DNA damage?

When oxidative stress occurs, ROS can react with DNA molecules, leading to the formation of DNA lesions. These lesions can include DNA strand breaks, base modifications, and DNA adducts. If left unrepaired, these DNA lesions can accumulate and result in mutations, genomic instability, and ultimately contribute to various diseases, including cancer and aging.

The impact of oxidative stress on DNA damage is primarily mediated through the generation of ROS, which can be produced by various cellular processes such as mitochondrial respiration, inflammation, and exposure to environmental factors like UV radiation and pollutants. ROS can directly damage DNA by causing chemical modifications to its structure or indirectly by interfering with the cellular machinery responsible for DNA repair.

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To counteract the detrimental effects of oxidative stress on DNA, cells have evolved multiple defense mechanisms. These include antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase, which help neutralize ROS and prevent their interaction with DNA. Additionally, cells possess DNA repair pathways, such as base excision repair and nucleotide excision repair, which can recognize and correct DNA lesions caused by oxidative stress.

However, excessive or chronic oxidative stress can overwhelm these defense mechanisms, leading to an accumulation of DNA damage. This can have severe consequences for cellular function and overall health, as damaged DNA can disrupt normal cellular processes and contribute to the development of age-related diseases.

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In conclusion, oxidative stress can impact DNA damage by generating reactive oxygen species that can directly damage DNA or interfere with DNA repair mechanisms. Understanding the mechanisms underlying oxidative stress-induced DNA damage is crucial for developing strategies to mitigate its negative effects and promote longevity and overall health.

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