摘要:There is general agreement that mitochondria play an important role in the aging process, but the role of mitochondrial oxidative stress remains controversial. Most previous work looking at mitochondrial oxidative stress has focused on damage to DNA, proteins, and lipids with age or in response to manipulation of cellular antioxidants. The interaction between oxidative damage and aging has been called into question in recent years by studies demonstrating little effect on aging and lifespan in mice with genetically modified antioxidant systems [1]. A notable exception is the life extension and protection against multiple diseases in mice that express catalase in the mitochondria, which suggests that the cellular location and type of reactive oxygen species is an important factor [2].