YAŞLANMA SÜRECİNDE MİTOKONDRİNİN ROLÜ
DOI:
https://doi.org/10.46291/ICONTECHvol4iss3pp1-10Keywords:
Mitochondrial DNA; mitochondrial; aging; free radicals; oxidative stresAbstract
ABSTRACT
Mitochondria are defined as the power centers of the cell that produce ATP, which is used in cellular functions. Mitochondrial dysfunction is an important part of the aging process. As the cells age, the efficiency of the respiratory chain decreases, electron leakage increases and ATP formation decreases. Different cell types have different numbers of mitochondria, and since they have their own DNA, they can divide independently of the cell they are in. In other words, mitochondrial replication is not dependent on cell division. During reproduction, half of a child's DNA comes from their father and half from their mother. However, the child always receives their Mitochondrial DNA (mtDNA) from their mother. The majority of mitochondrial diseases are caused by mutations in nuclear DNA that affect products that cause mitochondria. These mutations can be hereditary or spontaneous. When the mitochondria stop working, the cell they are in is deprived of energy. Therefore, symptoms can vary greatly depending on the type of cell. Cells that need the greatest amount of energy, such as heart muscle cells and nerves, are most affected by faulty mitochondria. 62 years ago, Harman suggested that aging is mediated by macromolecular damage caused by reactive oxygen species (ROS). ROS is produced in mitochondria as a byproduct of energy production, and these structures damage DNA, fats, and proteins. It is now focused on the target mitochondria in aging. Studies reveal that oxidative stress, mitochondrial DNA mutations, and a decrease in mitochondrial turnover mediate cellular aging. In this review, it is aimed to review the role of mitochondria in the human aging process on the basis of recent findings.
Key Words: Mitochondrial DNA; mitochondrial; aging; free radicals; oxidative stres
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