The history of the creation of Hayflick’s theory
Leonard Hayflick (born May 20, 1928 in Philadelphia), professor of anatomy at the University of California at San Francisco, developed his theory while working at the Wistar Institute in Philadelphia, Pennsylvania, in 1965. Frank MacFarlane Burnet named this theory after Hayflick in his book entitled Internal Mutagenesis, published in 1974. The concept of the Hayflick limit helped scientists study the effects of cell aging in the human body, cell development from embryonic stage to death, including the effect of shortening the length of the ends of chromosomes called telomeres.
In 1961, Hayflick began working at the Wistar Institute, where he observed through observation that human cells do not divide indefinitely. Hayflick and Paul Moorehead described this phenomenon in a monograph titled Serial Cultivation of Human Diploid Cell Strains. Hayflick’s work at the Wistar Institute was intended to provide a nutrient solution for the scientists who conducted experiments at the institute, but at the same time Hayflick was engaged in his own research on the effects of viruses in cells. In 1965, Hayflick elaborated on the concept of the Hayflick limit in a monograph titled “Limited Lifespan of Human Diploid Cell Strains in the Artificial Environment”.
Hayflick came to the conclusion that the cell is able to complete mitosis, i.e., the process of reproduction through division, only forty to sixty times, after which death occurs. This conclusion applied to all varieties of cells, whether adult or germ cells. Hayflick put forward a hypothesis according to which the minimum replicative ability of a cell is associated with its aging and, accordingly, with the aging process of the human body.
In 1974, Hayflick co-founded the National Institute on Aging in Bethesda, Maryland.
This institution is a branch of the US National Institutes of Health. In 1982, Hayflick also became vice chairman of the American Society for Gerontology, founded in 1945 in New York. Subsequently, Hayflick worked to popularize his theory and refute Carrel’s theory of cellular immortality.
Refutation of Carrel’s theory
Alexis Carrel, a French surgeon who worked with chicken heart tissue in the early twentieth century, believed that cells could reproduce indefinitely by dividing. Carrel claimed that he was able to achieve the division of chicken heart cells in a nutrient medium – this process continued for more than twenty years. His experiments with chicken heart tissue reinforced the theory of endless cell division. Scientists have repeatedly tried to repeat the work of Carrel, but their experiments have not confirmed the “discovery” of Carrel.
Criticism of Hayflick’s theory
In the 1990s, some scientists, such as Harry Rubin at the University of California at Berkeley, stated that the Hayflick limit only applies to damaged cells. Rubin suggested that cell damage could be caused by the cells being in an environment different from their original environment in the body, or by scientists exposing the cells in the lab.
Further research into the phenomenon of aging
Despite criticism, other scientists have used Hayflick’s theory as the basis for further research into the phenomenon of cellular aging, especially telomeres, which are the terminal sections of chromosomes. Telomeres protect chromosomes and reduce mutations in DNA. In 1973, the Russian scientist A. Olovnikov applied Hayflick’s theory of cell death in his studies of the ends of chromosomes that do not reproduce themselves during mitosis. According to Olovnikov, the process of cell division ends as soon as the cell can no longer reproduce the ends of its chromosomes.
A year later, in 1974, Burnet called the Hayflick theory the Hayflick limit, using this name in his paper, Internal Mutagenesis. At the heart of Burnet’s work was the assumption that aging is an intrinsic factor inherent in the cells of various life forms, and that their vital activity corresponds to a theory known as the Hayflick limit, which establishes the time of death of an organism.
Elizabeth Blackburn of the University of San Francisco and her colleague Jack Szostak of the Harvard Medical School in Boston, Massachusetts, turned to the theory of the Hayflick limit in their studies of the structure of telomeres in 1982 when they succeeded in cloning and isolating telomeres.
In 1989, Greider and Blackburn took the next step in studying the phenomenon of cell aging by discovering an enzyme called telomerase (an enzyme from the group of transferases that controls the size, number and nucleotide composition of chromosome telomeres). Greider and Blackburn found that the presence of telomerase helps body cells avoid programmed death.
In 2009, Blackburn, D. Szostak and K. Greider received the Nobel Prize in Physiology or Medicine with the wording “for their discovery of the mechanisms of protection of chromosomes by telomeres and the enzyme telomerase.” Their research was based on the Hayflick limit.