Hepatic Toxicity and Recovery of Fischer 344 Rats Following Exposure to 2-Aminoanthracene by Intraperitoneal Injection

Autor: Stephen P. Lee, Mary E.P. Goad, Steven A. Barker, David G. Baker, H. Wayne Taylor, Jay C. Means
Rok vydání: 2001
Předmět:
Adenoma
Male
0301 basic medicine
medicine.medical_specialty
medicine.medical_treatment
Intraperitoneal injection
Weight Gain
Toxicology
Disease-Free Survival
Pathology and Forensic Medicine
03 medical and health sciences
0302 clinical medicine
Albumins
Internal medicine
medicine
Animals
Aspartate Aminotransferases
Molecular Biology
Anthracenes
030102 biochemistry & molecular biology
business.industry
Biliary hyperplasia
Body Weight
Liver Neoplasms
Remission Induction
Albumin
Globulins
Blood Proteins
Cell Biology
Hyperplasia
Hepatocellular adenoma
Alkaline Phosphatase
medicine.disease
Rats
Inbred F344
Rats
Endocrinology
medicine.anatomical_structure
Liver
Biochemistry
Focal Nodular Hyperplasia
030220 oncology & carcinogenesis
Hepatocyte
Toxicity
Carcinogens
Alkaline phosphatase
business
Injections
Intraperitoneal
Mutagens
Zdroj: Toxicologic Pathology. 29:328-332
ISSN: 1533-1601
0192-6233
DOI: 10.1080/019262301316905282
Popis: Humans may be exposed to 2-aminoanthracen e (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 IP 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 ≥ 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.
Databáze: OpenAIRE
Externí odkaz: