ABSTRACT
This chapter provides biochemical data of mitochondria in cell aging and discusses the bioenergetic and physiopathological implications of age-related mitochondrial dysfunction. Mitochondrial injury occurs mainly in differentiated cells, and especially in neurons and other fixed postmitotic cells because they cannot regenerate their mitochondria as effectively as proliferating cells which renew their organelles each time they engage in mitosis. Senescent mitochondrial breakdown and energy loss may play a role in the genesis of age-related degenerative diseases of the somatic tissues mainly composed of fixed postmitotic cells, such as the cardiac and skeletal muscle and the CNS. Mitochondrial biogenesis could be impaired and a decline in ATP synthesis would occur in the tissues of aged individuals as the result of oxidative damage to the nuclear genome. An age-related impairment in mitochondria biosynthesis is also suggested by a computer-assisted morphometric study of the synaptic mitochondria of the cerebellar glomeruli of rats.
