Histopathological findings on Carassius auratus hepatopancreas upon exposure to acrylamide: correlation with genotoxicity and metabolic alterations

• Published in: Journal of applied toxicology 2014-12, Vol.34 (12), p.1293-1302
• Main Authors: Larguinho, Miguel, Costa, Pedro M., Sousa, Gonçalo, Costa, Maria H., Diniz, Mário S., Baptista, Pedro V.
• Format: Article
• Language: English
• Subjects: Acrylamide; Acrylamide - toxicity; Alterations; Animals; Carassius auratus; Chemicals; Comet Assay; CYP1A; DNA Damage; Dose-Response Relationship, Drug; Erythrocytes - drug effects; Erythrocytes - pathology; Exposure; Failure; Fish; Genetics; Genotoxicity; Glutathione Transferase - metabolism; goldfish; Goldfish - genetics; Goldfish - metabolism; GST activity; Hepatopancreas - drug effects; Hepatopancreas - metabolism; Hepatopancreas - pathology; Histopathology; Metabolism; Micronuclei, Chromosome-Defective - chemically induced; Micronucleus Tests; Microsomes, Liver - drug effects; Microsomes, Liver - metabolism; Microsomes, Liver - pathology; Organisms; pancreatic toxicity; Toxicity; Water Pollutants, Chemical - toxicity
• ISSN: 0260-437X; 1099-1263
• DOI: 10.1002/jat.2936

ABSTRACT Acrylamide is an amide used in several industrial applications making it easily discharged to aquatic ecosystems. The toxicity of acrylamide to aquatic organisms is scarcely known, although previous studies with murine models provided evidence for deleterious effects. To assess the effects of acrylamide to freshwater fish, goldfish (Carassius auratus L.) were exposed to several concentrations of waterborne acrylamide and analysed for genotoxic damage, alterations to detoxifying enzymes and histopathology. Results revealed a dose‐dependent increase in total DNA strand breakage, the formation of erythrocytic nuclear abnormalities and in the levels of hepatic cytochrome P4501A (CYP1A) and glutathione S‐transferase (GST) activity. In addition, acrylamide induced more histopathological changes to pancreatic acini than to the hepatic parenchyma, regardless of exposure concentration, whereas hepatic tissue only endured significant alterations at higher concentrations of exposure. Thus, results confirm the genotoxic potential of acrylamide to fish and its ability to induce CYP1A, probably as a direct primary defence mechanism. This strongly suggests the substance's pro‐mutagenic potential in fish, similarly to what is known for rodents. However, the deleterious effects observed in the pancreatic acini, more severe than in the liver, could indicate a specific, albeit unknown toxic mechanism of acrylamide to fish that overran the organism's metabolic defences against a chemical agent rather than causing a general systemic failure. Copyright © 2013 John Wiley & Sons, Ltd. The toxicity of acrylamide to aquatic organisms is scarcely known. Goldfish were exposed to several concentrations of waterborne acrylamide and the results showed a dose‐dependent increase in genotoxicity endpoints and in the levels of hepatic CYP1A and GST activity. In addition, acrylamide induced more histopathological changes to pancreatic acini than to the hepatic parenchyma. Overall, the findings suggest a specific mode of action that overran the defences against acrylamide a rather than causing a general systemic failure.