Because humans have a long lifespan relative to other organisms, aging studies have been performed in a variety of systems. Caenorhabditis elegans (C. elegans)
is one model organism that has been used to study aging due to its short life span (about 3 weeks), low cost for maintenance, its ease of cultivation and the fact that it produces large number of offspring [1-2]. The mechanisms involved in aging in C. elegans
have also been studied in other organisms, including mammals. Among these mechanisms are oxidative damage, dietary restriction, reduction in the Insulin/Insulin-like Growth Factor (IGF) signaling pathway and decreased TOR (Target of Rapamycin) signaling [1-4].
Oxidative damage in C. elegans
has been shown to play a prominent role in aging. The mev-1 mutants have increased production of reactive oxygen species and have shortened life spans  while daf-2 mutants that have increased antioxidant genes, including a gene for Superoxide Dismutase (SOD) and mutations in the Insulin /Insulin-like Growth Factor (IGF) receptor have longer life spans compared to wild type strains [1-3]. One study has found that when mbk-1 is lost, the lifespan of daf-2 is shortened. MBK-1 has been identified as a protein kinase .
Previous studies have shown that dietary restriction extends the lifespan of both C. elegansand
mammals [5-6]. Effects on the insulin-like growth factor signaling pathway and lysosomal degradation by autophagy are mechanisms involved with this life extension. ATG18 helps to maintain lifespan in C. elegans.
It has also been found that the mammalian homolog WIPI is involved with age-related human diseases . Other studies have looked at the effect of diet on longevity. Recent research with C. elegans
shows that diets high in glycogen decrease lifespan and accelerates the aging of the daf-2 worms that normally have an extended lifespan .C. elegans
is also a valuable organism to use to study aging since many mutant strains are available from the Caenorhabditis Genetics Center. Specific strains of C. elegans
can be found by searching the wormbase website but some examples can be found at this link: http://www.wormbase.org/search/gene/aging%20mutants
. Studies have also been done with C. elegans
to identify drugs that could delay aging both in these organisms and in mammals. Many of these drugs were found to increase the resistance to oxidative stress and target intracellular signaling .
Studies on aging in C. elegans
require synchronized populations to be used so that the animals are all of the same age. One common mechanism used is to treat the C. elegans
with bleach so that only the eggs remain. Then, the drug 5-fluoro-2’-deoxyuridine (FUdR) is used which kills diving cells so that the adult C. elegans
will remain but no further offspring will be viable. It is important, though, that the FUdR is administered to adults as the drug is toxic to young C. elegans.
In order to do the experiments, the timing of administering the C. elegans
is critical. The drug is toxic to larvae so the C. elegans
should be transferred to plates with the FUdR just before they start laying eggs. If it is given to the worms when they are young, the survival rate will be low. In addition, if the C. elegans
are too old, the hatched C. elegans
may be able to survive the drug treatment [1-2].