Hepatic toxicity and recovery of Fischer 344 rats following exposure to 2-aminoanthracene by intraperitoneal injection

• Published in: Toxicologic pathology Vol. 29; no. 3; p. 328
• Main Authors: Baker, D G, Taylor, H W, Lee, S P, Barker, S A, Goad, M E, Means, J C
• Format: Journal Article
• Language: English
• Published: United States 01.05.2001
• Subjects: Adenoma - chemically induced; Adenoma - pathology; Albumins - analysis; Alkaline Phosphatase - blood; Animals; Anthracenes - administration & dosage; Anthracenes - toxicity; Aspartate Aminotransferases - blood; Blood Proteins - analysis; Body Weight - drug effects; Carcinogens - administration & dosage; Carcinogens - toxicity; Disease-Free Survival; Focal Nodular Hyperplasia - chemically induced; Focal Nodular Hyperplasia - pathology; Globulins - analysis; Injections, Intraperitoneal; Liver - drug effects; Liver - pathology; Liver Neoplasms - chemically induced; Liver Neoplasms - pathology; Male; Mutagens - administration & dosage; Mutagens - toxicity; Rats; Rats, Inbred F344; Remission Induction; Weight Gain - drug effects
• ISSN: 0192-6233; 1533-1601
• DOI: 10.1080/019262301316905282

Humans may be exposed to 2-aminoanthracene (2-AA), a substituted polycyclic aromatic hydrocarbon, and a recognized mutagen and carcinogen, through oral and respiratory routes from contact with a variety of environmental sources. For the present study, we sought to evaluate hepatic damage and recovery in Fischer 344 rats following multiple i.p. injections of 5 mg of 2-AA. Rats were injected weekly for up to 5 weeks. Subgroups were then allowed to recover for 1, 5, or 9 weeks, and biochemical and pathologic changes were evaluated. We observed that weight gains were reduced relative to controls for all groups receiving > or = 2 injections. Serum enzyme levels indicative of liver damage were evident and included alterations in serum aspartate aminotransferase, alkaline phosphatase, total protein, albumin, and globulin. These alterations usually returned to normal by 5 weeks following cessation of 2-AA administration. In contrast, histologic liver changes, including hepatocyte hypertrophy, biliary hyperplasia with oval cell proliferation, altered foci, nodular hyperplasia, and one hepatocellular adenoma became more severe with time. This experiment demonstrates patterns of hepatic damage and recovery in rats exposed to 2-AA.