小鼠实验,线粒体DNA z-bo 2020-11-05 604

　　To some extent, a person’s lifespan may even be determined before they are born, if a study published in Scientific Reports on October 9, 2014 turns mice into humans. This new study suggests that mutations in mitochondrial DNA in a mother’s egg cells may shorten her child’s lifespan by about one-third.

　　"The extreme importance of this kind of work is to prove that mitochondrial DNA (maternal inheritance) carries genetic information that is vital to longevity," said Douglas Wallace, professor of pathology and laboratory medicine at the Children's Hospital of Philadelphia. Wallace was not involved in this new study, but he independently showed that maternally inherited mitochondrial gene mutations can affect aging, longevity and cancer.

　　This new article is based on an article published last year in the journal Nature. That article showed that, in other wild-type mice, mutations in the mitochondrial DNA from the mother are sufficient to cause premature aging-a discovery that was a disease of Yale University. Gerald Shadel, professor of science and genetics, described it as "a real breakthrough."

　　But because of the eagerness to publish this new discovery. "We didn't know whether their lifespan was affected," said Jaime Rose of the Karolinska Institute, the first role of the two papers Scientific Reports and Nature. Because it takes about a year to wait for the animal to die.

　　Now, compared to the control group with an average lifespan of 141 weeks, the average lifespan of mice that inherited mutant mitochondrial DNA is 100 weeks. Douglas Turnbull, professor of neurology at Newcastle University (who was not involved in the study), described the result as "interesting but not surprising" because prematurely aging animals will die young.

　　However, I don’t know why mitochondrial DNA mutations shorten the life span. Mitochondrial dysfunction may affect cell metabolism and cause various problems, such as the accumulation of harmful reactive oxygen species, reduced stem cell viability, and reduced DNA repair, leading to the accumulation of damage in the nuclear genome. "Aging is a complex process and involves so many different aspects," Ross said. "So, all of this comes together little by little and keeps beating the organism in a short period of time."

　　But regardless of the mechanism of action or mechanism, damaged mitochondria can affect aging. This finding points out that this mutation can lead to a cross-generational effect with reproductive effects. Wallace said that, for example, mitochondrial mutations tend to accumulate as a person's body tissues age, and it can also be thought that this process may also occur in egg cells. If so, older women pass on more mitochondrial gene mutations to their offspring than younger mothers.

　　"If, we can theoretically measure these mutations, we can say to ourselves, well, if they get a higher threshold than the mother's egg cells, then what else can we do?" Ross said. "Maybe intervention." She said, maybe medicine or nutrition may help. Just like three-parent in vitro fertilization—a technique that enables a woman with a severely disease-causing mitochondrial gene mutation to inject a nucleus from her egg cell into a healthy woman’s Egg cells (that is, carrying unaffected mitochondria) to avoid passing the disease to offspring. This technology is expected to be available in the UK within a few years.

　　People who have inherited the state of mitochondria do not have to worry. There is evidence that premature aging exercises in mice carrying mitochondrial gene mutations can delay the aging process. "We can change our destiny, which is good news," Rose said.