Among the byproducts of mitochondrial energy production are "reactive oxygen species" that include hydrogen peroxide-the same hydrogen peroxide used as an antiseptic and hair bleach. (In fact, the bleaching action of hydrogen peroxide is visible evidence of its oxidative power.) Many of these reactive oxygen species are free radicals. The free radicals include superoxide and the deadly hydroxyl radical (the same type of free radical that is produced in nuclear explosions). Oxygen free radicals, unless they are quickly neutralized by antioxidants, can cause considerable damage to the membranes of mitochondria and to mitochondrial DNA. The injury caused by these free radicals initiates a self-perpetuating cycle in which oxidative damage impairs mitochondrial function, which results in the generation of even greater amounts of oxygen free radicals.

Over time, the affected mitochondria become so inefficient, they are unable to generate sufficient energy to meet cellular demands. Mitochondria from older individuals tend to be less efficient than those from younger cells.

Mitochondria appear, then, to be an obvious focus of study for researchers who study aging. Their role as energy producers makes them absolutely crucial to the life of the cell. But they also produce threateningly large quantities of oxygen free radicals. As the source of these toxic products, mitochondria are also their first potential victims. Their proximity to the free radicals they produce, combined with their exceedingly intricate structure, make them particularly vulnerable to oxidative injury over time.

Mitochondrial DNA is not as well protected as nuclear DNA, which is coated with proteins. The "naked" mitochondrial DNA becomes an easy target for rogue reactive oxygen species. In a recently published study in Circulation Research, Scott Ballinger and colleagues at the University of Texas Medical Branch in Galveston found that when cultured animal cells were exposed to various types of oxygen free radicals, their mitochondrial DNA was more severely damaged than their nuclear DNA. Another study found that mitochondrial DNA damage was more extensive and persisted longer than nuclear DNA damage in human cells following oxidative stress. In general as cells age, the number of gaps and errors in their mitochondrial DNA tends to increase, and oxidant exposure is the likely cause. Controlling oxidative damage, therefore, appears to be one strategy for defeating some of the effects of aging.

As the body ages, we absorb nutrients less efficiently, and this can affect the efficiency of mitochondrial function. Cardiolipin is a component of the energy producing process that is found almost exclusively in mitochondria. Cardiolipin levels naturally decline with age. Lipid peroxidation, a type of oxidant damage more common in older cells, leads to a decrease in cardiolipin. Cardiolipin itself can suffer the effects of lipid peroxidation, and the progressive accumulation of crippled cardiolipin molecules is yet another way in which oxidant damage can jeopardize the efficiency of energy production.

Coenzyme Q10, also known as CoQ10 or ubiquinone, is another factor necessary for energy production. It is available in the diet and it can be manufactured from simpler precursors. CoQ10 deficiency can affect brain and nerve function, and aging skeletal muscle cell mitochondria contain less of this important factor than do mitochondria from younger cells.
Carnitine, an amino acid, is also important to mitochondrial metabolism because it helps chaperone fatty acids into the mitochondria, where they can be metabolized. Carnitine deficiency leads to an inability to harvest the energy stored in fatty acids and to a build-up of fatty intermediates that can prove toxic to cells. Again mitochondria from older cells tend to contain less carnitine.