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New research shows reducing exposure to common chemicals may slow aging

Researchers at Nagoya University in Japan discovered that aldehydes are metabolic byproducts associated with premature aging. published Nature Cell Biology The findings reveal insights into diseases of premature aging and potential anti-aging strategies such as controlling exposure to aldehyde-causing substances such as alcohol, pollution and smoke in healthy people.

Aldehydes can harm human health. But the team’s findings suggest that these harmful effects also involve aging. The team that made this discovery included Yasuyoshi Oka, Yuka Nakazawa, Mayuko Shimada and Tomoo Ogi from Nagoya University.

“DNA damage is associated with aging phenotypes,” Oka said. “But we propose for the first time that there is a link between aldehyde-induced DNA damage and premature aging.”

The connection between aldehydes and aging

Researchers have suggested that there may be a link between aldehydes and aging because people with premature aging disorders such as AMeD syndrome show deficient activity of enzymes such as ALDH2 that break down aldehydes.

In healthy people, ALDH2 is also important in our response to alcohol. When a person drinks wine or beer, the liver converts the alcohol into aldehydes, allowing them to be eliminated from the body. ALDH2 activity is important for the conversion of aldehydes into a non-toxic substance.

Aldehydes are harmful because they are highly reactive with DNA and proteins. In the body, they form DNA-protein cross-links (DPCs) that block important enzymes in typical processes such as cell proliferation and maintenance, causing malfunctions in these processes and aging of the patient.

Focusing on aldehyde-induced DPCs, scientists used a method called DPC-seq to investigate the relationship between aldehyde accumulation and DNA damage in prematurely aging patients. In a series of experiments, the researchers found that the TCR complex, VCP/p97, and the proteasome play a role in the removal of formaldehyde-induced DPCs from actively transcribing regions. This was confirmed with a mouse model lacking both aldehyde clearance processes and the TCR pathway, which showed worse symptoms of AMeD syndrome.

These processes are important because they are involved in the purification of aldehydes. This indicates a link between premature aging diseases and aldehyde accumulation.

Research results and future directions

Professor Augie said he was looking forward to the results of his findings: “By elucidating the mechanism that enables rapid repair of DNA damage, we have uncovered part of the cause of genetic premature aging.”

“Our study opens new avenues for understanding the mechanisms underlying diseases of premature aging and offers potential targets for therapeutic intervention,” Oka said. said. “By elucidating the role of aldehydes in DNA damage and aging, we pave the way for future research to develop new treatments and interventions.”

He continued: “Therapeutic development has not progressed because we do not fully understand the causes of AmeD syndrome and Cocaine syndrome. This study suggests that the patient’s condition is associated with DPC derived from aldehydes produced in cells. “These results are expected to aid the search for compounds that scavenge aldehydes and thus facilitate the development of therapeutic drug candidates.”

This research has implications beyond genetic diseases; because their findings suggest that aldehyde-induced DNA damage may play a role in the aging process in healthy people. By identifying aldehydes as age-promoting agents, this study sheds light on the complex relationship between environmental factors and cellular aging. This can have significant consequences for a person’s health and life expectancy.

Source: Port Altele



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