Functional elucidation of food materials targeting organ aging

Abstract

Mitochondria are the site of aerobic energy production and the base of production of reactive oxygen species (ROS). Age-related decline in mitochondrial function is a target of anti-aging research because it affects cell fate. Superoxide (O₂·-), the base substance of ROS generated by physiological oxygen metabolism in mitochondria, is promptly treated by the catalytic action of superoxide dismutase (SOD). In the cell, SOD1 is constitutively localized in the cytoplasm and SOD2 in the mitochondrial matrix, respectively, and the intracellular O₂·- level is appropriately maintained. Analyses using genetically engineered mice revealed that disruption of redox regulation due to cytoplasmic SOD1 or mitochondrial SOD2 deficiencies causes cell death and senescence-like phenotypes in cells, leading to atrophy and dysfunction in various organs throughout the body. Since both mouse models exhibit premature aging and age-related diseases, they are aging model mice based on oxidative damage. In addition, since the models also show clear age-related organ phenotypes, it is considered possible to scientifically evaluate drugs and food factors. In this review, I would like to introduce the latest knowledge of model mice and specific examples of functional food factors, and discuss the possibility of aging control.