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THE INDUCTION OF ABERRANT CRYPT FOCI (ACF) IN MALE AND FEMALE F344/N RATS BY BROMOCHLOROACETIC ACID (BCA) ADMINISTERED IN THE DRINKING WATER
Citation:
George, M H., D. A. Delker, D. R. Geter, A B. DeAngelo, C. Herbert, J. H. Roycroft, R. L. Melnick, AND D. Rosenberg. THE INDUCTION OF ABERRANT CRYPT FOCI (ACF) IN MALE AND FEMALE F344/N RATS BY BROMOCHLOROACETIC ACID (BCA) ADMINISTERED IN THE DRINKING WATER. Presented at AACR, Orlando, Florida, March 27-31, 2004.
Description:
The Induction of Aberrant Crypt Foci (ACF) in Male and Female F344/N Rats by Bromochloroacetic Acid (BCA) Administered in the Drinking Water.
M.H. George1, D. Delker1, D.R. Geter1, C.Herbert2, J. Roycroft3, R. Melnick3, D.W.
Rosenberg4, and A.B. DeAngelo1. 1USEPA, Research Triangle Park, NC, 2Southern
Research Institute, Birmingham, AL, 3NIEHS, Research Triangle Park, NC, and 4University
of Connecticut, Farmington, CT.
BCA, a by-product of chlorine disinfection (DBP), is found in the the lower parts per billion ( g/L) in finished drinking water. Male and female F344/N rats were exposed to 250 (low), 500 (mid), and 1000 (high) mg/L BCA dissolved in deionized water (vehicle control). After
26 and 52 weeks of exposure to BCA in the drinking water, the colons were examined for the presence of ACF, the putative preneoplastic precursors of colorectal neoplasia. Males. The incidence (percent of animals with an ACF) and multiplicity (ACF/animal ? SD) of ACF in male rats were increased only in the high BCA exposure group at 26 weeks (88%; 2.13 ? 0.55 vs 13%; 0.13 ? 0.13 for the control) and at 52 weeks (88%; 2.88 ? 0.61 vs 25%; 0.25
? 0.16 for the control). Females. A significant induction of ACF was observed in females exposed to low (88%; 1.38 ? 0.26), mid (100%; 2.38 ? 0.53), and high (75%; 4.13 ? 1.25) BCA when compared to the control (13%; 0.13 ? 0.13) at 26 weeks. At 52 weeks, ACF were enhanced in the low (88%; 2.5 ? 0.71), mid (100%; 3.0 ? 0.95), and high (100%; 8.63 ? 2.40) BCA exposure groups when compared to the control (25%; 0.25 ? 0.16). Female rats were more sensitive than males to ACF induction by BCA and the number of ACF increased with the length of exposure in the high BCA treatment group. We had previously demonstrated the induction of ACF by dibromoacetic acid (unpublished observation) and brominated trihalomethanes (DeAngelo, A. et al, 2002, Cancer Letters, 187, 25-31). The incidence of ACF induced by brominated trihalomethanes was maximum at 26-52 weeks, but regressed with continued exposure and only an occasional colorectal neoplasia was observed at the end of the two year study (Sistrunk, C. and DeAngelo, T., 2001. Internatl. J.Toxicol., 20,408-409). ACF induced by brominated haloacetic acids and trihalomethanes are being compared with ACF induced by azoxymethane, a colon carcinogen, with respect to molecular markers that characterize progression to colorectal cancer. This is an abstract of a proposed presentation and does not necessarily reflect EPA policy.