In a new study, researchers find that alcohol can damage DNA in stem cells.
This could help explain why drinking increases risk of cancer.
Previous research looking at the precise ways in which alcohol causes cancer has been done on the cell level.
But in the current study, the researchers show how alcohol exposure leads to permanent genetic damage.
They gave diluted alcohol, chemically known as ethanol, to mice.
They used chromosome analysis and DNA sequencing to examine the genetic damage caused by a harmful chemical produced when the body processes alcohol.
They found that the chemical acetaldehyde could break and damage DNA within blood stem cells, and that it caused rearranged chromosomes and permanently altering the DNA sequences within these cells.
It is known that when healthy stem cells become faulty, they can give rise to cancer.
The finding can help people to understand how drinking alcohol increases the risk of developing 7 types of cancer including breast and bowel cancer.
In addition, the study examined how the body tries to protect itself against damage caused by alcohol.
The team found that the first line of defense is enzymes called ALDH. These enzymes break down harmful chemicals into acetate, which our cells can use as a source of energy.
Some people either lack these enzymes or carry faulty versions of them.
When they drink, the harmful chemical builds up which causes a flushed complexion, and also leads to them feeling unwell.
The second line of defense is a variety of DNA repair systems. Most of the time, the systems allow them to fix and reverse different types of DNA damage.
But they don’t always work, and some people carry mutations which mean their cells aren’t able to carry out these repairs effectively.
Scientists at the MRC Laboratory of Molecular Biology (link is external), Cambridge conducted the study. Professor Ketan Patel is the lead author of the study.
This research was funded by Cancer Research UK, Wellcome and the Medical Research Council (MRC).
The study is published in Nature.
Source: MRC
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