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INDUCTION OF URINARY BLADDER PATHOLOGY IN MALE AND FEMALE C3H MICE EXPOSED TO SODIUM ARSENITE FROM GESTATION THROUGH YOUNG ADULTHOOD
Citation:
AHLBORN, G., R. GRINDSTAFF, J. W. ALLEN, G. M. NELSON, K. T. KITCHIN, M. H. GEORGE, J. PRESTON, M. WAALKES, B. DIWAN, AND D. A. DELKER. INDUCTION OF URINARY BLADDER PATHOLOGY IN MALE AND FEMALE C3H MICE EXPOSED TO SODIUM ARSENITE FROM GESTATION THROUGH YOUNG ADULTHOOD. Presented at 2007 Society of Toxicology Annual Meeting, Charlotte, NC, March 25 - 29, 2007.
Description:
Epidemiology studies suggest that chronic exposure to inorganic arsenic is associated with cancer of the skin, urinary bladder and lung as well as the kidney and liver. Recently, an in utero animal model was developed to characterize the carcinogenic properties of inorganic arsenic (Waalkes et al., 2003). A brief exposure to sodium arsenite in utero (gestation day 8 to 18, GD8- 18) increased liver, lung, adrenal, ovarian and uterine tumors in C3H and/or CD-1 mice. In the study described here, C3H mice were exposed to 85 ppm inorganic arsenic in their drinking water in utero (GD8-18) or a similar brief exposure post-pubescence (postnatal day 57 to 67, PD57-67) or a prolonged continuous exposure through both stages of development (GD8-PD67). At PD67, groups (n=5) of male and female mice from control and all treatment groups were examined pathologically. Body weights were significantly lower (~15%) in mice continuously exposed to arsenic when compared to controls. No treatment-related differences in food consumption were observed. A treatment-related increase in eosinophilic granules of the urinary bladder transitional epithelium was observed in all male and female mice of the prolonged continuous (GD8-PD67) and brief post-pubescence exposure groups (PD57-67). These eosinophilic granules are representative of degradative products in response to injury. The severity of bladder lesions was greatest in the GD8-PD67 group followed by the PD57-67 group. One female mouse in the in utero only exposure group also demonstrated minimal eosinophilic granule accumulation in the bladder epithelium. Uterine hyperplasia was observed in two female mice in the continuously exposed group and one female mouse in the PD57-67 treatment group. These results demonstrate that a brief exposure, in utero or post-pubescence, to sodium arsenite is sufficient in inducing aberrant changes in urinary bladder and/or uterine pathology in mice and that prolonged exposure from gestation through young adulthood increases the severity/incidence of these lesions.