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Di(isononyl) phthalate (DINP) and di(isodecyl) phthalate (DIDP) are not mutagenic
Author(s) -
Mckee Richard H.,
Przygoda R. T.,
Chirdon M. A.,
Engelhardt G.,
Stanley M.
Publication year - 2000
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/1099-1263(200011/12)20:6<491::aid-jat724>3.0.co;2-h
Subject(s) - phthalate , micronucleus test , genotoxicity , carcinogen , clastogen , micronucleus , biology , toxicology , cancer research , medicine , toxicity , chemistry , genetics , organic chemistry
Abstract Recently there have been reports of liver and kidney tumors in rodents following long‐term exposure to di(isononyl) phthalate (DINP). Mechanistic studies suggested that the liver tumors were a consequence of peroxisomal proliferation, whereas the kidney tumors (found only in male rats) were associated with induction of α 2u ‐globulin. Because both peroxisomal proliferation and α 2u ‐globulin are considered to be non‐genotoxic carcinogenic processes, it seemed appropriate to investigate the genotoxic potential of DINP. Additional studies were also conducted on di(isodecyl) phthalate (DIDP), a structurally related substance that also induces peroxisomal proliferation, although it has not been tested in a carcinogenicity bioassay. The DINP was tested in Salmonella , in vitro cytogenetics and mouse micronucleus assays, whereas DIDP was evaluated in a mouse micronucleus test. All of these tests produced negative results, i.e. neither phthalate was mutagenic in any of the test systems. These data are consistent with results of other published and unpublished genotoxicity tests and provide support for the hypothesis that the liver and kidney tumors induced by DINP were the result of non‐genotoxic processes. Copyright © 2000 John Wiley & Sons, Ltd.