Ageing is the process of becoming older. Generally speaking, the term refers especially to human beings, many animals, and fungi. Cell aging is the result of physical and chemical assaults, of molecular exhaustion, and of physiological attempts to compensate for damage. Examples include toxic adducts to macromolecules, attrition of chromosomes, DNA damage, and impaired organelles.
Metabolic changes are hallmarks of aging and genetic and pharmacologic alterations of relevant pathways can extend life span. Among these pathway, the fundamental theory of ageing is ROS.
ROS, also known as reactive oxygen species, are by-products of the respiratory chain in the inner mitochondrial membrane, where redox reactions create a proton gradient that drives ATP generation. Superoxide radicals are produced by complex (I) and complex (III) of the respiratory chain.
Three scavenging mechanisms (including superoxide dismutase [(SOD), mitochondrion and cytosol], catalase (peroxisome), and glutathione peroxidase (mitochondrion and cytosol)) act in a stepwise fashion to remove these radicals. First, SOD detoxifies the superoxide and creates hydrogen peroxide. This intermediary can form the more dangerous hydroxyl radical if not removed. Catalase and glutathione peroxidase prevent hydroxyl radical formation by converting hydrogen peroxide into water. Increased SOD activity without changes to catalase or glutathione peroxidase can be harmful due to accumulation of damaging hydroxyl radicals.
Increased ROS production through desynchronized respiration or lower ROS scavenging capacity with age offers an attractive model to explain damage to proteins through carbonylation or to DNA through guanine modifications. With their proximity to the respiratory chain, mitochondrial proteins and mitochondrial DNA that lacks protective nucleosomes are especially prone to damage.
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