In the long history of scientific research, there have been many key discoveries that overturned people's traditional concepts. In the 1960s, with the discovery of the Hayflick limit, the limit of cell division, by American anatomist Leonard Hayflick, the scientific community's understanding of cell lifespan changed dramatically. However, prior to this, research by French surgeon Alexis Carrel claimed that cells are immortal, a conclusion that remains controversial to this day. Why were subsequent scientists unable to replicate Carrel's experimental results? What secret is hidden behind this?
Carrel's research is full of mystery. He once claimed that he could continue to culture fibroblasts from chicken hearts in a culture environment, even reaching a life span of 34 years.
This claim was challenged in Hayflick's experiments. His experiments showed that normal human fetal cells divide only 40 to 60 times in culture, and then enter the senescence stage. This discovery not only refuted Carrel's theory, but also showed that cellular aging is closely related to the aging of the entire organism.He believes that all cells transplanted into tissue culture are immortal, and the reason why cell division stops is simply due to imperfect culture techniques.
After Hayflick became skeptical of Carell's claims, he began an in-depth study of the cell behavior he had observed. He found that during the culture process, some cells showed unusual characteristics after dividing about 40 times, and the division rate slowed down significantly.
Working with Paul Moorhead, they discovered that cell division behavior in mixed cultures provides conclusive evidence that the arrest of cell division is controlled by an internal computational mechanism.He ruled out factors such as possible contamination, poor culture conditions, and unknown experimental errors, and designed a complete experiment to verify the internal mechanism of cell senescence.
Although Carrel's experiment received great attention, subsequent scientists were never able to replicate his results. There are several possible reasons behind this. One view is that Karel's cell culture may not be carried out in the usual way.
In addition, some scholars have suggested that the cells used by Karel may be in a relatively young state. If they can be combined with nutrients that promote telomerase activation, they will be able to delay the aging process or even reverse aging. This is has not received enough attention.For example, he may have added chicken embryonic stem cells to provide necessary nutrients, and actually continuously cultured new cells instead of the original ones. Infinite proliferation of cells.
Telomeres are DNA sequences located at both ends of chromosomes, which play a vital role in cell division. Each time a cell divides, telomeres gradually shorten in length. Hayflick pointed out for the first time that the ability of normal cells to divide is clearly related to the length of telomeres. When telomeres shorten to a critical value, cells will enter the senescence stage.
This also explains why Hayflick was able to verify that normal cells have a life limit, while cancer cells show immortal characteristics.The reason why cancer cells are able to proliferate indefinitely is because they express an enzyme called telomerase, which can lengthen telomeres and thereby prevent cell aging.
Hayflick's discovery brings new understanding of the human aging process. He believes that the limited ability of cells to divide is closely related to the aging of the overall organism. Many studies have found that the body's non-stem cells divide far less often than cells observed in the laboratory. This prompts a rethinking of the human need for cell division during aging and how these biological mechanisms manifest themselves in different body cells.
Hayflick's discovery not only changed the biological community's understanding of cell lifespan, but also promoted in-depth research on the mechanisms of aging. As science advances, our understanding of cells, cancer, and aging will continue to evolve. Will we find solutions to slowing aging in the future, or is this just an age-old problem?