A Catalogue of Shame
Six groups of 12-week old female rats were used to test a new compound for treating radiation burns. All of the rats were anaesthetised and received a burst of radiation to the underside of the tongue, resulting in mouth ulcers.
The rats were subsequently allowed to recover from the anaesthetic. One subgroup received no treatment whatsoever, while the remaining five received various combinations of the treatment compound. No animals died before the end of the experiment, but no mention is made of the fate of the rats thereafter. The authors concluded that more experiments should be carried out, in which the rats would receive repeated doses of radiation, rather than a single burst.
Modification of radiation-induced acute
oral mucositis in the rat.
International Journal of Radiation Biology 2004, vol. 80(2): 177-182.
Rezvani M, Ross G.
Research Institute, University of Oxford
The 'rat model' used in the above experiment is simply a repetition of an earlier mouse model used to demonstrate the same principle. Instead of studying, and deliberately harming, mice and rats, scientists would do much better focusing on the many human cases of radiation-induced mucositis (inflammation of the lining of the mouth and digestive system produced as a result of radiotherapy treatment). They could do so by beginning with human cell culture studies, and eventually progressing to actual patients.
Researchers at the University of Oxford compared three monkeys with artificially produced brain damage, with a human subject whose brain was damaged in an accident.
The monkeys were three adult rhesus macaques. Two had had parts of their brains removed 10 years previously, when they were five years old. The third monkey, already aged 14 years, was operated on recently and given six months to recover before being tested. The human subject was 48 years old, but suffered brain damage when he was eight years old. The monkeys and the human were subjected to tests that measured reaction time to a visual stimulus. At the end of the tests, the researchers concluded that the human subject never managed to respond as fast as the fastest monkey. They also could not determine why one monkey behaved differently from the others.
Chromatic priming in hemianopic visual fields.
A Cowey, P Stoerig, I Hodinott-Hill. Experimental Brain Research 2003; 152:95-105.
Funding: Medical Research Council.
The long-term experimental use and incarceration of these monkeys must expose them to extreme distress and suffering. This is another clear example where the law offers no protection. Paragraph 14 of the Animals (Scientific Procedures) Act of 1986 states that, where an experimental animal has been subjected to regulated procedures, or has been given a general anaesthetic and allowed to recover consciousness, 'it shall not be used for any further regulated procedures'.
However, this apparent protection falls away, since this section of the paragraph does not apply if the initial procedure (e.g. major surgery) is simply a preparation for subsequent procedures.
Two macaque monkeys were used to mimic Parkinson's disease in humans. The experiment involved injecting a chemical, which affects nerve transmission, directly into their brains. They were also injected intravenously with a second chemical, called MPTP, which produced Parkinson-like tremors.
The researchers noted, from previous experiments performed by other scientists, that greater brain damage results in more severe behavioural symptoms. Depending on the dose of MPTP, the monkeys experienced varying degrees of incapacity, tremors, rigidity and loss of voluntary body movements. Parkinson's disease in humans is caused by poorly understood death of dopamine producing cells in the brain. It has absolutely nothing to do with MPTP. In addition, Parkinson's disease does not occur naturally in monkeys. In the final stage of this experiment, both monkeys were given a large dose of MPTP, which essentially froze them in their tracks. The animals were allowed to suffer the debilitating effects of this drug for ten days, during which time they required intensive nursing to keep them alive. At various stages during the experiment, the monkeys received a drug (orally, or by injection into the brain) to reverse, or reduce, the experimentally-induced symptoms. The aim of the experiment was to examine the effect of injecting a chemical directly into the part of the brain whose malfunction is associated with Parkinson's disease symptoms. At the end of the experiment, both animals were killed.
Reversal of akinesia in experimental parkinsonism
by GABA antagonist microinjections in the pedunculopontine nucleus.
Nandi D, Aziz T, Giladi N, Winter J, Stein J. Brain 2002; 125: 2418-2430.
University laboratory of physiology, Oxford University.
Funding: Medical Research Council (UK) and Norman Collisson Foundation.
One must question the very reason for this experiment. A fundamental difference between Parkinson's disease in humans and 'monkey models' of the disease, is that, while humans get progressively worse, monkeys gradually recover from the condition.
Two adult male rhesus monkeys were trained to fixate their vision on a small point for several seconds. Once they had learned the task, they were anaesthetised and had a metal coil implanted near the eye, which was wired up to record eye movements. They were also fitted with a head restraint and recording chamber over a part of the brain that had been exposed to allow recording of brain cell activity.
During the experiment, the monkeys were positioned in a primate chair with their heads forcibly restrained. They were required to fixate their vision on different patterns. In addition, the monkeys had to press and release a lever within a very short period of time in exchange for water reward. Giving the monkeys small amounts of water as a 'reward' would suggest that they were deprived of water before the experiment. Brain cell activity was then recorded. The authors concluded that different brain cells respond to different patterns seen by the monkeys. No mention was made of what was done with the monkeys after the termination of the experiment.
Pattern motion is present in V1 of awake
but not anaesthetised monkeys.
European Journal of Neuroscience, 2004, Vol. 19: 1055-1066.
Guo K, Benson P, Blakemore C.
University laboratory of physiology, University of Oxford.
Funding: Medical Research Council (UK), Oxford MRC centre in brain and behaviour, the Oxford McDonnell-Pew centre for cognitive neuroscience, the US Air Force Office of scientific research, European office of aerospace research and development.
Scientists and non-scientists alike agree that research funds are a scarce resource. It is therefore a travesty that this sort of activity should be funded at a time when so many human patients are not receiving the medical attention that they need.
Although the specific purpose of this research is not mentioned in the paper, it is both noteworthy and disturbing to see that military bodies participated in its funding.
The advancement of knowledge for its own sake does not justify inflicting pain and suffering on sentient creatures. Nor does the law provide any meaningful protection for these laboratory animals. Animal experimentation is not about science or helping human beings through meaningful, rational research. It is about the search for grants, academic prestige and career development.
At a time when the scientific validity of animal experimentation is increasingly questioned from within the research community itself, it is time for thinking scientists to publicly challenge the relevance of such experiments.
This concludes Oxford University and Animal Experimentation: A Catalogue of Shame. To find out how you can help see the latest action alerts.