The body is subject to constant assault from outside toxins such as pollutants - DDT, dioxin, cigarette smoke and so on. But surprisingly, a large number of toxic compounds are generated from within. Among the most troublesome of these compounds are substances called oxidants thrown off by mitochondria, the powerhouses that convert fuel into energy (i.e., they change nutrients into useful molecules that the body can use). The oxidants produced by mitochondria can be just as damaging to vital cellular components as any outside hazard.

Virtually any part of the cell can be affected - proteins, lipids, and nucleic acids (DNA and RNA). DNA, the main substance of our genes, is particularly at risk. DNA strands must be accurately duplicated every time a cell divides - an extremely demanding process. Our cells use DNA to create the proteins that do a wide range of physiological jobs. Mistakes or mutations introduced into DNA can give rise to errant proteins that don't perform efficiently or which might not work at all. Sometimes, the DNA of a cell becomes so riddled with errors and gaps that it cannot duplicate, and the cell dies. DNA damage can also cause the death of cells that are not duplicating.

But of all cellular constituents, perhaps the most vulnerable are the very same mitochondria that produce most of the offending oxidants. Mitochondria, like the nuclei of cells, contain DNA that is vital to their function. But mitochondria also possess a very elaborately structured membrane that is important in energy production. The elements of this membrane must act with a precision that is relatively unforgiving of injury or disruption.

The healthy human organism is prepared to deal with the errors and injury inflicted by rogue chemicals - so long as the damage is not too severe. Detoxifying factors continually confront and neutralize highly reactive chemicals. While this process of cellular hygiene - the finding of errors and the neutralization of toxins - is efficient, it is not perfect. Inevitably, some errors go uncorrected, causing molecular mistakes to pile up. In fact, a theory that has gained considerable standing among some life scientists is that aging is the visible result of the gradual accumulation of damaged cellular components and unrepaired mistakes.

But if aging represents an accumulation of mistakes and injury, might it be possible to slow the process by reducing such damage? Many researchers believe that slowing the rate of aging is an achievable goal. And some have focused upon controlling mitochondrial oxidant damage as a means of achieving it. Bruce Ames, a prominent researcher at the University of California, Berkeley, has summarized the importance of mitochondria in aging this way: "Aging appears to be due, in good part, to the oxidants produced by mitochondria as by-products of normal metabolism."