In an investigation of this concept, Lin et al. (1998) identified a mutant methuselah gene that enhances the resistance of the common fruit fly (Drosophila melanogaster) to various forms of stress and enables it to live about 35% longer than normal.  They also note that other strains of fruit flies that display delayed senescence exhibit enhanced abilities to withstand the stresses of heat, desiccation, food deprivation and oxidative tissue damage; and they cite related studies of mutant lines of the nematode Caenorhabditis elegans that also live longer than normal, presumably as a result of enhanced resistance to thermal and oxidative stresses.

What do these findings have to do with the air's CO2 concentration?  No one really knows; but we note that atmospheric CO2 enrichment tends to confer these same stress-withstanding abilities upon plants (see the many sub-headings under Growth Response to CO2 with Other Variables in our Subject Index); and these observations prompt us to ask what few people have ever thought to explore: Is there a common thread that links these biochemical phenomena across the vast expanse that separates plants from animals, such that animals as well as trees (see Life Span (Plant) in our Subject Index) may be similarly benefited and find their lives lengthened and their health bettered as the air's CO2 content continues to climb?

This question may sound a bit strange, like something to be found on the fringes of science; but consider these words from Paul Berg (Cahill Professor of Cancer Research and Director of the Beckman Center for Molecular and Genetic Medicine at Stanford University) and Maxine Singer (Scientist Emerita at the National Cancer Institute and President of the Carnegie Institution of Washington), which they wrote in an Essay on Science and Society in the same issue of Science that contained the report of Lin et al.:

"Molecular genetics has revealed a wealth of detail about many biological systems.  Still, current ignorance is vaster than current knowledge.  ... There are, in nature, concepts that no one has yet imagined.  Looking over the past 150 years ... it seems that the fringes, not the mainstream, are the most promising places to discover revolutionary advances."

Keeping these thoughts in mind, we find some reinforcement for them in the work of Larsen and Clarke (2002), who fed diets with and without coenzyme Q to wild-type nematodes (Caenorhabditis elegans) and several mutants during the adult phases of their lives, while they recorded the lengths of time they survived.  As they describe their observations, "withdrawal of coenzyme Q (Q) from the diet of wild-type nematodes extends adult life-span by ~60%."  They also report that the life-spans of the four different mutants they studied were extended by a Q-less diet.  More detailed analyses of their results led them to conclude that the life-span extensions were due to reduced generation and increased scavenging of reactive oxygen species.

The results and conclusions of this study are similar to those of Melov et al. (2000), who also studied C. elegans, testing the theory that reactive oxygen species cause aging by examining the effects of two superoxide dismutase-/catalase-like mimetics (EUK-8 and EUK-134) on the life-spans of normal and mutant C. elegans worms that ingested various amounts of the mimetics.  In every experiment, treatment of normal worms with the antioxidant mimetics significantly increased both mean and maximum life-span.  Treatment of normal worms with but 0.05 mM EUK-134, for example, increased their mean life-span by fully 54%; and in mutant worms whose normal life-span was genetically shortened by 37%, treatment with 0.5 mM EUK-134 restored their life-span to normal by increasing their mutation-reduced life-span by 67%.  It was also determined that these effects were not due to a reduction in worm metabolism, which could have reduced the production of oxygen radicals, but "by augmenting natural antioxidant defenses without having any overt effects on other traits."

Melov et al. say their results "suggest that endogenous oxidative stress is a major determinant of the rate of aging."  The significance of this statement resides in the fact that antioxidants tend to reduce such stresses in animals, and in the observation that atmospheric CO2 enrichment has been shown to significantly enhance the concentrations of many of these plant constituents (see Antioxidants in our Subject Index), as well as the concentrations of several substances that have been proven effective in fighting a number of cancers, viral infections and other animal maladies (see Health Effects (Carbon Dioxide) in our Subject Index).

Do these observations suggest that the rising CO2 content of earth's atmosphere will enable animals to live longer?  Maybe not; but who knows what a few well-conceived research programs designed to probe this question might ultimately reveal.  There are enough tantalizing correspondences turning up in the fields of CO2 and animal aging research that they almost beg to be seriously scrutinized within this context.

References
Berg, P. and Singer, M.  1998.  Inspired choices.  Science 282: 873-874.

Finkel, T. and Holbrook, N.J.  2000.  Oxidants, oxidative stress and the biology of ageing.  Nature 408: 239-247.

Larsen, P.L. and Clarke C.F.  2002.  Extension of life-span in Caenorhabditis elegans by a diet lacking coenzyme Q.  Science 295: 120-123.

Lin, Y.-J, Seroude, L. and Benzer, S.  1998.  Extended life-span and stress resistance in the Drosophila mutant methuselah.  Science 282: 943-946.

Melov, S., Ravenscroft, J., Malik, S., Gill, M.S., Walker, D.W., Clayton, P.E., Wallace, D.C., Malfroy, B., Doctrow, S.R. and Lithgow, G.J.  2000.  Extension of life-span with superoxide dismutase/catalase mimetics.  Science 289: 1567-1569.