Animal carcinogen testing challenged
Article Abstract:
Many of the man-made chemicals are potential carcinogens (cancer-causing agents). Researcher Bruce Ames of the University of California, Berkeley and others have claimed that the risk of many of the chemicals has been overestimated partly due to a flaw in the design of animal tests used to evaluate the carcinogenicity of the substances. Ames and Lois Swirsky Gold established the Carcinogenic Potency Database in the early 1980s, which now contains 4,000 experiments assessing the carcinogenicity of approximately 1,000 chemicals in rodents. They found that more than half (over 500) of the chemicals were reported to cause cancer. They feel that this percentage is too high and is the result of a flaw in the testing procedure. The chemicals are given to animals in maximum tolerated doses (MTDs), which are the highest doses that can be given without severe toxic reactions. These doses represent much larger concentrations than man would be exposed to. Ames feels that the doses are too high and at these doses, the chemicals have more subtle, but real, toxic effects. The high doses kill some cells, causing other cells to divide to make up for the cell loss. The increased cell division raises the chances that mutations, or genetic changes, will occur, which increases the risk of cancer. Ames feels that below the toxic dose, cell division would not occur and cancer would not develop. Other scientists, including John Bailar of McGill University and I. Bernard Weinstein of Columbia University's College of Physicians and Surgeons, do not agree with Ames's views. Scientists at the National Institute of Environmental Health Science and those at the Environmental Protection Agency emphasize that the results of the animal testing represent only one of several factors they consider when assessing the potential carcinogenicity of substances. Ames also points out that there are many natural carcinogens that people ingest in their diets. Man has evolved defenses to protect against the natural carcinogens, and these defenses can probably work against synthetic chemicals as well. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1990
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Expanded HIV-1 cellular tropism by phenotypic mixing with murine endogenous retroviruses
Article Abstract:
Researchers attempting to understand the AIDS (acquired immunodeficiency syndrome) virus and potential treatments for it are working to develop animal models for the human disease. At first, monkeys appeared most promising because of their similarity to humans, but various species that have been experimentally infected have shown no evidence of developing the immune deficiency associated with AIDS. Scientists are also investigating smaller animals such as mice. A special genetically-mutated strain of mice is being studied; these animals have a severe deficiency of their own immune system and, through transplantation, can be given human immune cells as a substitute. In this way the mice become a type of 'living laboratory' in which to study the human immune system infected with HIV (human immunodeficiency virus). But a major flaw in the mouse model was discovered by the authors. In the living animal, mouse viruses interacted with HIV type 1 (HIV-1) and this interaction caused important changes in the biological properties of HIV-1. The variants of HIV-1 that were produced may not be worth studying, because they do not function in the same way as the human AIDS virus. This casts doubt on the relevance of previous AIDS research done with some animal models. In addition, the authors note that mice infected with HIV-1 could pose a health hazard if they manufactured new forms of HIV; these new forms might be more potent infectious agents than the type of human AIDS virus now known. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1990
User Contributions:
Comment about this article or add new information about this topic:
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