Origins and consequences of mitochondrial decline in nucleated erythrocytes

Erythrocytes have many roles in ion regulation and respiratory gas exchange, processes that depend upon energy provided by mitochondrial metabolism. Within a few months after red cells are released into the circulation, they exhibit changes in structure and function. Aging is accompanied by reduced membrane fluidity, losses in organelles and a reduction in gene expression and protein synthesis. The impact of cellular aging on the responsibilities of erythrocytes has only recently been studied. We have previously shown that erythrocytes defend ion and gas exchange properties as they age (1). Conversely, aging has a profound effect on the ability of cells to mount heat shock responses (2). Recent work has focused on the impact of age-dependent changes in mitochondria and bioenergetics. Aging erythrocytes experience dramatic losses in mitochondria. These changes could reduce the capacity of the older erythrocytes to perform energy dependent functions. Age-induced changes in mitochondria could also increase the vulnerability of aged cells to mitochondria-initiated programmed cell death, or apoptosis