Meanwhile, in the interests of providing some substantive content in this thread, I'll expand a little on the known links between certain biomolecules, ageing and death.

Oxygen is a vital respiratory gas for a large number of multicellular eukaryote species (of which we are one). Quite simply, if a human being is deprived of oxygen, death follows in pretty short order. Indeed, the toxicity of cyanide is due to a process of chemical asphyxiation, brought about by the binding of cyanide ions to haemoglobin, producing a stable compound that is no longer able to engage in oxygen transport. Once oxygen transport to tissues via haemoglobin is shut down, death occurs in a matter of minutes.

But, despite the vital nature of oxygen for our life processes, there's a dark side to this essential molecule. Oxygen's vital role in eukaryote metabolism, hinges upon its reactivity. Its reactivity with glucose, mediated by ATP, provides the energy for organisms to continue living, as this reaction is exothermic, and liberates spare bond energy that can be used further along the metabolic chain, so to speak. However, that reactivity is not selective: the same oxygen molecules that react with glucose, and provide us with useful energy for the rest of our life processes, will also react with other molecules - many other molecules. This includes molecules whose structure and stability are important contributors to cellular life processes - disrupt those molecules, and cellular life processes start to become compromised. Oxygen will readily form a number of reactive species in vivo, including damaging superoxide ions, hydroxy radicals, and other, similar chemical species that are disruptive to metabolic processes if not controlled. In short, the oxygen you need to live, is slowly killing you at the same time - a useful lesson in toxicology.

Needless to say, living organisms have, over evolutionary time, acquired ways and means of reducing the damage wrought by reactive oxygen species, in the form of various antioxidant enzymes such as superoxide dismutase (SOD) and various catalases. Although control of reactive oxygen species is not, by any means, the only factor that has an impact upon longevity, it has been established to be a significant contributor by various lines of experimental work. For example, there exists a gene in Drosophila melanogaster fruit flies (and, for that matter a whole raft of other organisms) which, because of its effects upon longevity, has been named methuselah (biologists have long been renowned for a certain whimsical sense of humour when naming genes), usually shortened in the literature to mth.

It transpires that there exist mth mutant strains of D. melanogaster, which exhibit an extended life span compared to that of non-mutant flies. These long lived flies not only exhibit an extended life span, but also exhibit increased resistance to oxidative, heat and starvation stresses. In particular, mth mutant files exhibit enhanced resistance to the effects of paraquat, a compound used as a herbicide that is also toxic to animals. The toxicity of paraquat to animals, arises from the fact that this compound generates large quantities of reactive oxygen species in vivo, overwhelming the antioxidant defences of animal cells, and leading via this process to rapidly lethal disruption of vital mitochondrial function. However, whilst D. melanogaster individuals with a 'normal' genotype succumb quickly to paraquat poisoning, mth mutant flies exhibit considerably enhanced resistance to paraquat, by virtue of the operation of the mutant mth gene. The mutant mth gene results in the production of a protein that possesses its own, additionally enhanced capacity for removing reactive oxygen species from the cytoplasm, but also upregulates the production of other antioxidant enzymes such as SOD, resulting in mth mutant flies producing a much more abundant army of antioxidants to control wayward reactive oxygen species. This results in reduced oxidative damage to critical metabolic pathways, and as a corollary, an enhanced lifespan.

It's worth noting that homologues of mth, and variations in the genes coding for SOD and catalases, are frequently correlated with lifespan. Organisms with relatively inefficient variations on the theme tend to be short lived, whilst long-lived organisms have more efficient variations. This is not the whole story with respect to longevity, of course, but the insights from biochemistry and molecular biology in this vein are worth noting.

A long dissertation on the subject of the mth gene and its mutations can be found here. It transpires that another useful by-product of mth involves modified and beneficial (from a longevity standpoint) integration with insulin signalling. For a full exposition of the state of knowledge of this subject, one is invited to track down the 21 scientific paper references at the end of that article.

I could cover, in a similar vein, how other molecules that are considered vital nutrients, such as glucose, also have a dark side. Those like myself, who have to deal with type 2 diabetes, become aware of this dark side in an immediately manifest visceral manner. The same glucose molecules you need to power your body, will over time reveal their dark side, through such means as their long term implication in atherosclerosis, for example. Similarly, triglycerides (the chemical family to which fats belong) have their own woes associated with them, and cholesterol, which is of such ubiquitous metabolic utility that our bodies synthesise it, will also reveal its propensity for chemical mischief over time given the opportunity.

In short, with life, comes death, and it comes precisely because of the varied nature of the chemical reactions we rely upon to live.