There are two kinds of people: bunny huggers (Mukerjee, 1997) and cruel scientists (Barnard & Kaufman, 1997; Mukerjee, 1997). The overzealous bunny huggers (BH) argue that animal research is wasteful because animals are bad model organisms and deserve ethical treatment. The cruel scientists (BS) argue that animal research is necessary to scientific advancement because animals are good model organisms, and may be used after an in-depth cost-benefit analysis. Both of these arguments are seriously flawed because they are biased, emotional, and incomplete. This paper will offer a balanced approach to animal experimentation.
There are three persuasive arguments against animal research. First, the lab environment and methodology are very stressful for animals. Many lab animals experience isolation and enclosure. This unnatural lifestyle causes pain and suffering for subjects. The official web-site for PETA, a prominent BH organization, cites many cases where lab animals are placed under excessive pain, distress, and isolation. A second BH argument explains that animals are not good model organisms. For example, advancement in polio research was delayed because in vivo results misled researchers. A second example is that for many years, cigarettes were considered harmless because non-human primates react less to cigarette smoke. In both of these cases, many human lives were lost because the model organisms used did not accurately represent humans. The third BH argument is that there are many in vitro alternatives to in vivo. In the past, chemicals were tested for corrosiveness in vivo; synthetic skins, though, nearly eliminated the need for in vivo tests.
On the other hand, there are compelling proponents of animal research. The most persuasive CS argument is that animal research has led to tremendous human benefit. Research into dendritic cells has generated many novel new cancer medications with no adverse effects and complete tumor elimination (Antoni et al, 200). Animal research was necessary before Phase I clinical trials to test for autoimmune development. A second CS argument ascertains that certain animals are model organisms. For example, rats are considered “genetic stunt doubles†to humans, and results from rat studies have been successfully extrapolated onto humans. (Pearce, 1999) Rats and humans share 85% of the same gone, and rats are anatomically anthropomorphic. The third CS argument is that animal research is carefully regulated by both scientists and non-scientists. This ensures that animal research is conducted only if there is a low cost/benefit ratio. In addition, in places where animal research is conducted there is a department devoted to supervision. This third argument states that although there is although lab animals will always undergo some form of suffering, the benefit that arises will outweigh their sacrifice.
A compromise for BH’s and CS’s would discriminate between primates, rodents, invertebrates, plants, and microbes, and require rodent testing before primate testing. Primates, which undergo the most humanlike emotional transformations, require the most supervision and regulation. In-depth analysis and meta-analysis of animal research could give insight into which scenarios had low cost/benefit ratios. In addition, more literature review might occasionally eliminate the need for primates. By examining outliers (ie, rodents) then solid results with less variables can be generated. Rodent experiments, which are most common, are necessary for examining systemic diseases. For example, tumors cannot be fully studied in vitro because countless variables influence results. While rodent experiments require as much supervision as primate experiments, regulation should be more lenient. The third group of subjects, invertebrates, requires very little ethical intervention. The primary consideration with invertebrates is maintenance and disposal. It is important that invertebrates are maintained well for hygienic and ethical reasons, and they must be disposed of respectfully and cleanly (ie, not piled up in an alley behind CHS). However, since invertebrates lack the sophisticated vertebrate view of reality, many factors influencing vertebrate research—such as discomfort, isolation, and pain—are not as important. Fourthly, the only regulation necessary for plant research involves disposal. The cost of plant maintenance motivates research to treat the plants optimally. In addition, wasteful plant research will not get funding and will cease. However, plants still viable after research should be donated for domestic enjoyment. Lastly, microbes should be treated the same as plants. Since some microbes are pathogenic, though, a culture should be Clorox-washed before being tossed into a toxic waste. Essentially, financial factors will ensure that plants and microbes are not wasted.
In conclusion, there are both legitimate and illegitimate components of the animal research debate. Compromise is essential if the benefits of animal research are to dominate the costs to the creatures involved.
References
Anti, R. et al. (2000). Generation of T-Cell Immunity to a Murine Melanoma Using MART-1-Engineered Dendritic Cells. Retrieved January 13, 2006. http://www.immunotherapy-journal.com/pt/re/jimmuno/abstract.00002371-200001000-00008.htm;jsessionid=DR5nv2xvNXj0GCNth2416JcOlV3417gEJVYrviM5WYQQB5wqgMoi!1871300765!-949856144!9001!-1
Barnard, N. and Kaufman, S. (1997). Animal Research is Wasteful and Misleading. Retreived January 18, 2006. http://mipwww.life.uiuc.edu/404%20Docs/SciAm% 20articles/AnmResrchProCon.pdf
Mukerjee, M. (1997). Trends in Animal Research. Retreived January 18, 2006. http://mip www.life.uiuc.edu/404%20Docs/SciAm%20articles/AnmResrchProCon.pdf
Pearce, J. (1999). Of Mice and Men. Retrieved October 17, 2004,
http://www.ornl.gov/info/ornlreview/rev27-12/text/mnmmain.html
Rowan, A. (1997).. The Benefits and Ethics of Animal Research. Retreieved January 18, 2006. http://mipwww.life.uiuc.edu/404%20Docs/SciAm%20articles/AnmResrchProCo n.pdf
The cells of a 25 year old are not youthful. The chromosome has been degraded, leading the person rapidly toward a life dominated by wrinkles, sedentariness, and AARP. Telomeres are short repetitious chromosomal sequences. They prevent the degradation of the chromosome during DNA replication that is terminated early. When the telomere sequence becomes too short, the cell is unable to safely replicate its DNA and thus halts replication. As the cell becomes old, though, it becomes inefficient and will eventually die (this is a causative agent of aging). To restore the telomeres, most cells use an enzyme called telomerase. This enzyme attaches new strands of telomere to the 5’ end of the chromosome. Telomeres, which are a vital part of the chromosome, are vital to regulation of cell cycles, aging, and tumor development.
Telomeres are 5’ repetitious 8-10 base-pair sequences. Since DNA Polymerase terminates DNA replication before reaching the end of the template, the telomeres sacrifice themselves so that the rest of the DNA is fully replicated. Once telomeres become too short, however, newly replicated strands have no protection from premature termination. As a result, cells with too-short telomeres enter senescence, a phase during which they do not replicate. Extended senescence, though, results in reduced efficiency of the cell. It gradually becomes unhealthy and will eventually die without replacing itself. Fortunately, a polymerase named Telomerase extends the telomeres. This, in turn, prevents senescence. Telomerase carries its own template strand in the form of RNA. In this manner, it can replicate the telomere sequence beyond the chromosomal template.
Loss of telomere length might be a causative agent of aging. Guo-Liang Yu, of Blackburn laboratory, demonstrated in 1990 that immortality is dependent upon telomerase in Tetrahymena. Telomerase mutants lose cell mass and die. Similarly, other members of the Blackburn laboratory have observed similar degradation in other species of Telomerase mutants. Similarly, if Telomerase activity is low or absent in human cells then after a period of time the human body will undergo a similar process (shrinkage followed by death). Human newborn somatic cells divide 80 to 90 times in culture, while somatic cells from a 70 year old divide only 20 to 30 times. After division ceases, senescence occurs. During senescence, cells under morphological transformations and begin operating less efficiently. In addition, Greider, Harley and their colleagues observed that most normal somatic cells lost telomere segments during incubation. This means that Telomerase was not active. Similarly, Greider, Harly, and Hastie (of Medical Research Council in Edinburgh) found that telomeres in some human tissues shorten with age.
A treatment could be generated to exploit the connection between aging and telomere length. Since Telomerase is known to regenerate telomerase, then CMV-Telomerase could be transduced via a non-specific adenoviral vector into most eukaryotic cells. This would give the host cells the ability to encode Telomerase, which would then regenerate telomeres. In conjunction with a hormonal treatment to encourage cell proliferation, the cells would be able to exit senescence. Daughter cells would operate more efficiently than their ancestors, thus giving the patient a more youthful look. Such a medication would have tremendous benefit for the elderly, as it could have tremendous benefit physically. Mentally, though, the effect would be negligible since neuron proliferation is rare. For example, an ideal candidate might be a 25-year-old patient suffering from wrinkling, indigestion, and age-related discomfort. After being infected, the patient might notice that youth has been reinstated within just a few months. This treatment would have many risks, though, for it might induce immortality and lead to the development of tumors. A way to prevent Telomerase-related cancer development might be to encode a CMV-Telomerase promoter activator that is cleaved by Hfl protease (present during high cellular metabolic activity, as in cancer cells).
In conclusion, telomere loss leads to aging, and this process can be reversed by telomerase. Telomerase treatment might have great therapeutic and cosmetic benefits, but it also provides an environment hospitable to cancer. As a result, genetically engineering the human body to look young is currently a bad way to reverse the effects of aging. A good way is a face-lift.
References
Greider, E. & Blackburn, H. (1996). Telomeres, Telomerase and Cancer. Scientific American, February 1996. Retrieved February 1st from http://www.genethik.de/telomerase.htm
