repair machinery as does the DNA in the cell nucleus. Regardless of whether free radical levels are causing harm in this way, they are also important to the operation of metabolism through other channels. Different longevity-inducing mutations have been noted to either raise and lower the normal levels of free radical generation in various species. So on the one hand it is argued that hormetic effects cause a boost in repair mechanisms throughout the cell, producing a net benefit despite more free radicals running around, while on the other hand its also argued that reducing levels of free radicals leads to less damage in the first place and thus much the same net benefit.Equally, any or all of these longevity mutations could be extending life through other mechanisms that have less to do with free radicals: there is a lot of room yet for theorizing even though the mainstream consensus heavily favors oxidative damage as an important mechanism. Understanding the operations of the cell is a complex business for individual cells, never mind a whole body full of them.The importance of this present research quoted below is as a reference system, one that can be ported to other species to generate better hard data on what exactly is going on with regard to free radical levels across a life span. That will make it much easier in the years ahead to pin down cause and effect in a variety of mechanisms related to mitochondria - I can immediately think of half a dozen things I'd like to see tested in conjunction with a form of this technology ported to mice.Lifespan predicted from flashes in worm cellsQuote:[Researchers] added proteins to nematode worms that fluoresce when they detect damaging free radical molecules in their mitochondria. Mitochondria generate a cell's energy. It's long been thought that an accumulation of free radicals, produced when cells metabolise, drives the ageing process by damaging DNA and proteins. Mitochondria are particularly at risk because they produce free radicals in large quantities but lack the DNA repair mechanisms found in other parts of the cell.[The] team found that the number of "mitoflashes", caused by the presence of free radicals, emitted when a nematode was three days old could predict its lifespan. Worms typically live for 21 days and are at their peak of reproductive fitness at 3 days old. Those with low mitoflash activity at that time lived longer, while those with high mitoflash activity died before day 21.Worms carrying a genetic mutation known to extend life to 39 days exhibited fewer mitoflash bursts than genetically healthy worms, and free radical production peaked later in their lifespan. Conversely, worms with a life-shortening mutation exhibited much higher than average mitoflash frequency which peaked earlier.The same pattern was seen when the team exposed the worms to short periods of starvation and heat shock, environmental stresses that counter-intuitively increase lifespan, and to a toxic herbicide known to shorten lifespan.Mitoflash frequency in early adulthood predicts lifespan in Caenorhabditis elegansQuote:It has been theorized for decades that mitochondria act as the biological clock of ageing, but