A team of researchers at Nagoya University in Japan has made a significant discovery regarding the impact of aldehydes on DNA damage and aging. Their findings, published in Nature Cell Biology, shed light on the association between aldehydes and premature aging diseases, as well as potential strategies to mitigate aging in healthy individuals.
The study revealed that aldehydes, which are metabolic byproducts, are linked to premature aging. The researchers emphasized the importance of controlling exposure to aldehyde-inducing substances such as alcohol, pollution, and smoke to combat aging in healthy individuals.
The team, led by Yasuyoshi Oka, Yuka Nakazawa, Mayuko Shimada, and Tomoo Ogi of Nagoya University, highlighted the relationship between aldehyde-derived DNA damage and premature aging. They hypothesized this connection based on the inadequate activity of enzymes like ALDH2 in individuals with premature aging disorders.
ALDH2 plays a crucial role in metabolizing alcohol into non-toxic substances in the body. The researchers emphasized the significance of ALDH2 in converting aldehydes, which are highly reactive with DNA and proteins, into non-toxic substances. Aldehydes form DNA-protein crosslinks (DPCs) in the body, leading to the malfunction of essential cell maintenance processes and ultimately causing premature aging.
The study utilized a method called DPC-seq to investigate the link between aldehyde accumulation and DNA damage in premature-aging disease patients. The researchers identified key processes involved in the removal of formaldehyde-induced DPCs, emphasizing their association with premature aging diseases and aldehyde accumulation.
Professor Ogi expressed optimism about the implications of their findings, emphasizing the potential for developing strategies to combat premature aging diseases and mitigate aging in healthy individuals.
