Alcohol and mutations
Anti-cancer protein protects the embryo from pathologies
...and alcohol prevents him from doing it
Kirill Stasevich, Science and Life (nkj.ru )
The anti—cancer protein is BRCA1, which helps to stitch breaks in DNA and correct mutations of another kind. If the mutation gets into BRCA1 itself, there will be a threat of cancer, and most often we hear about BRCA1 in connection with malignant breast tumors.
But BRCA1 is also involved in other molecular processes — if you count the number of other proteins with which it interacts, there will be more than fifty of them. In particular, as they write in the journal Redox Biology, the staff University of Toronto (Drake, Wells, Novel mechanisms in alcohol neurodevelopmental disorders via BRCA1 depletion and BRCA1-dependent NADPH oxidase regulation) BRCA1 suppresses the activity of the NOX enzyme. This enzyme produces reactive oxygen species — aggressive oxidizing molecules that damage proteins, DNA and lipids. We usually hear about reactive oxygen species in connection with oxidative stress and are used to considering them something unambiguously bad. But they are also used by immune cells to fight bacteria and other pathogens, in other words, aggressive oxygen oxidizers are a kind of immune chemical weapons.
However, if the NOX enzyme becomes too active, it begins to harm the cells themselves. BRCA1 controls the activity of NOX, and the smaller the BRCA1, the more reactive oxygen species appear. That is, BRCA1 protects DNA not only by helping to repair damage that has already occurred, but also by trying to prevent these damages that occur due to oxygen radicals. But alcohol additionally suppresses the protective properties of BRCA1.
The researchers experimented with mice that served as a model of fetal alcohol syndrome, or fetal alcohol syndrome, — the so-called congenital abnormalities in the development of a child caused by the fact that the mother abused alcohol before and during pregnancy. It is known that these deviations are associated with oxidative DNA damage. Fetal alcohol syndrome in mice was assessed by the behavior of cubs born to mothers who were given alcohol.
Brain development and, accordingly, oddities in the behavior of the cubs depended on whether they had a lot of BRCA1 protein during embryonic development. If there was not enough of it, then even without any alcohol, the mice were born with neurological abnormalities. They could be avoided if the level of oxygen radicals from NOX was artificially lowered — that is, the connection between BRCA1 and NOX was obvious. If pregnant mice were given alcohol, the BRCA1 level dropped, and oxidative radicals from NOX that damaged DNA became more.
Perhaps the same thing happens in humans. If everything is confirmed, it will be possible to think about how to stimulate BRCA1-antioxidant protection in pregnant women with BRCA1 deficiency caused by genetic causes or environmental factors.
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