The Mechanism of ROS Treatment in Long-Lived Animals

Long-lived animals, like humans, are produced ROS in mitochondria. In mitochondria, longevity animals first prefer the metabolism of reducing ROS production. Then, they have various gene groups that rapidly remove the generated ROS. DNA damage occurs when ROS is released into the cytoplasm and attacks DNA in the nuclear envelope. Even though weak DNA damage, cell apoptosis pathways are activated and repair pathways are suppressed in longevity animals If the repair path is activated by light damage, it would lead to carcinogenesis by neglecting the mutation. Longevity animals efficiently treat ROS from metabolic processes and induce the activity of genes involved in apoptosis even in nuclear DNA damage. Longevity animals rapidly remove mutagenic cells through the cell death pathway to create an environment for cell neoplasia and to minimize cellular senescence as much as possible.