Wolf D C, Carlton W W
Department of Veterinary Pathobiology, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907.
Food Chem Toxicol. 1990 May;28(5):351-60. doi: 10.1016/0278-6915(90)90109-z.
Dose-response and sequential studies of 2-bromoethylamine hydrobromide (BEA) nephrotoxicosis were carried out using Swiss ICR mice. For the dose-response study, 150 male mice, 30 per group, were injected intraperitoneally (ip) with 100, 200, 300, 400 or 500 mg BEA/kg and ten from each group were killed 1, 3 or 5 days after treatment. For the sequential study, 80 male mice were injected ip with 300 mg BEA/kg and ten were killed at 0.5, 1, 2, 3, 6, 12 or 18 hr, or 10 days after treatment. Control mice (10-15) in both studies were given 0.15 ml of 0.9% NaCl solution injected ip and were killed after 1, 3 or 5 days in the former study and after 18 hr of 10 days in the latter study. Mortality and the extent of the renal lesions were dose dependent. The percentage of mice with tubular necrosis varied from 0 in mice given 100 mg BEA/kg to 100 in mice given 400 mg BEA/kg. The percentage of mice with renal papillary necrosis was also dose dependent and varied from 0 in the 100 mg/kg group to 72 in the 400 mg/kg group. Degeneration of proximal tubules was detected 2 hr after treatment. Three hours after treatment, grossly, the renal cortex was diffusely pale and, microscopically, there was marked acute tubular necrosis. Epithelial cells lining the cortical tubules were regenerating 3 days after treatment. By 10 days after treatment cortical interstitial fibrosis was marked with many tubules lined by regenerating epithelium and many tubules were dilated. BEA-induced nephrotoxicosis in the mouse was primarily an acute cortical tubular necrosis.
