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Rodent bioassay

Brown SJ, Raja AA, Lewis DFV. A comparison between COMPACT and Hazardexpert evaluations for 80 chemicals tested by the NTP/NCI rodent bioassay. ATLA 1994 22 482-500. [Pg.493]

Matthew EJ, Spalding JW, Tennant RW (1993) Transformation of BALB/c-3T3 cells via transformation responses of 168 chemicals compared with mutagenicity in salmonella and carcinogenicity in rodent bioassays. Environ Health Perspect 101 347 182... [Pg.151]

Cohen SM (2004) Human carcinogenic risk evaluation an alternative approach to the two-year rodent bioassay. Toxicol Sci 80 225-229... [Pg.109]

There has been extensive debate and consideration on the relevance and value of the traditional long-term rodent bioassays. The FDA looked at rat and mouse studies for 282 human pharmaceuticals, resulting in the conclusion that sufficient evidence is now available for some alternative in vivo carcinogenicity models to support their application as complimentary studies in combination with a single two-year carcinogenicity study [emphasis added] to identify trans-species tumorigens (Contrera et al., 1997). [Pg.300]

Is the proper comparator data for evaluating performance human or rodent bioassay data It should be kept in mind that there are sets of rodent bioassay... [Pg.318]

There may be situations which warrant an assessment of carcinogenic potential, but immunogenicity and species specificity may preclude a two-year rodent bioassay. It may be necessary to develop in vitro assays to address a particular concern. For example, growth factors which may have the potential to support or stimulate the growth of transformed cells should be assessed for their ability to promote growth of either malignant or normal cells. [Pg.439]

Brusick D. 1983. Evaluation of chronic rodent bioassays and Ames assay tests as accurate models for predicting human carcinogens. In Milman HA, ed. Application of biological markers for carcinogen testing, 153-163. [Pg.62]

None of three US industry-based case-control studies suggested an association between exposure to hydrogen chloride and cancers of the lung, brain, or kidney. This result was consistent with a rodent bioassay in... [Pg.388]

Kerckaert, GA., Brauninger, R., LeBoeuf, R.A. Isfort, R.J. (1996) Use of the Syrian hamster embryo cell transformation for carcinogenicity prediction of chemicals currently being tested by the National Toxicology Program in rodent bioassays. Environ. Health Perspect., 104 (Suppl. 5), 1075-1084... [Pg.500]

Unfortunately, there has been an uncritical acceptance of the notion that a positive result in a rodent bioassay automatically implies a carcinogenic risk for humans. While this may well be the case for genotoxic agents, for nongenotoxic substances there will be exceptions, especially if the proliferative response occurs only at high doses" (Cohen and Ellwein 1991, 903). [Pg.79]

Lave, Lester B., Fanny K. Eimever, Herbert S. Rosenkranz, and Gilbert S. Omenn. 1988. Informational Value of the Rodent Bioassay. Nature 336 631-33. [Pg.89]

It seems likely that a high proportion of all chemicals, whether synthetic or natural, would be carcinogens if administered in the standard rodent bioassay at the MTD, primarily because of the effects of high doses on cell death and division and DNA damage and repair.6 Without additional data about how a chemical causes cancer, the interpretation of a positive result in a rodent bioassay is highly uncertain. The induction of cancer could be the result of the high doses tested and have no predictive value about what might occur at lower doses. [Pg.132]

Evaluation or Re-evaluation of Some Agents Which Target Specific Organs in Rodent Bioassays... [Pg.1589]

The main tool to assess the carcinogenic potential of a chemical is the rodent bioassay. Because of its central role in the regulation of chemicals, the rodent bioassay has been under intense scrutiny. The overall evidence points to the validity of the bioassay as a basis for human risk assessment (Fung et al., 1995 Haseman et al., 2001 Huff, 1999 Huff, 2002 Tomatis et al., 1997). [Pg.183]

In addition to the rodent bioassay, the aromatic amines have been studied in the shorter term test Salmonella typhimurium mutagenicity as well as in a variety of acute toxicity assays. A number of QSARs have been generated from such data. The work of Hansch in recent years has demonstrated that the comparison of the QSAR models obtained in different systems, by putting them in a wider perspective, can provide useful clues in the study of the mechanisms of action of individual chemical classes, and can give precious hints on how appropriate the specific models and parameters selected are (Hansch, 2001 Hansch et al., 2002). An exercise of the mechanistic comparison of QSARs has been performed on aromatic amines (Benigni and Passerini, 2002). The results are detailed below. [Pg.190]

Bakale, G. and McCreary, R.D., Prospective Ke screening of potential carcinogens being tested in rodent bioassay by the US National Toxicology Program, Mutagenesis, 7, 91-94, 1992. [Pg.198]

Jones, J.D. and Easterly, C.E., On the rodent bioassays currently being conducted on 44 chemicals a RASH analysis to predict test results from the National Toxicology Program, Mutagenesis, 6, 507-514, 1991. [Pg.199]

Over the past decade other concerns have been raised about the continued use of rodent data and its relevance for predicting human risk [11-16], For example, more than half of the chemicals evaluated in the rodent bioassay have tested positive in one or more rodent species. One explanation has been that the large doses that are tested (i.e., maximum tolerated doses) may overwhelm the body s natural detoxification mechanisms. Cyclosporin A (CyA), a pharmaceutical used clinically as an immunosuppressant, is nongenotoxic (or... [Pg.401]

Factors Considerations When Rodent Bioassays Performed Not Needed... [Pg.407]


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See also in sourсe #XX -- [ Pg.539 ]




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