| Texto completo | |
| Autor(es): |
Bavia, Lorena
[1, 2]
Número total de Autores: 1
|
| Afiliação do(s) autor(es): | [1] Univ Sao Paulo, Inst Biomed Sci, Sao Paulo - Brazil
[2] Univ Fed Parana, Dept Med Pathol, Lab Mol Immunopathol, R Gen Carneiro 181, BR-80060900 Curitiba, Parana - Brazil
Número total de Afiliações: 2
|
| Tipo de documento: | Artigo Científico |
| Fonte: | JOURNAL OF PHARMACOLOGICAL AND TOXICOLOGICAL METHODS; v. 108, MAR-APR 2021. |
| Citações Web of Science: | 0 |
| Resumo | |
Acetaminophen (APAP) is commonly used to treat fever and pain. However, when in overdose is the predominant cause of hepatotoxicity. Despite advances in understanding the mechanisms of APAP-induced hepatotoxicity, the management of acute liver failure remains a challenge. Thus, more relevant experimental models are crucial to provide a better understanding of this condition. The aim of this study is to evaluate the effect of APAPinduced hepatotoxicity on A/J mice using C57BL/6 as reference experimental model. Eight- to ten-week-old male A/J and C57BL/6 mice were treated with APAP (300 or 500 mg/kg) by intraperitoneal injection. After 24 h total blood leukocyte counting, plasma levels of alanine amino transferase (ALT) and aspartate amino transferase (AST), histopathological analysis of liver, lung and kidney were evaluated. A/J mice presented reduction in circulating leukocytes concomitant with the increase in plasma levels of ALT and AST, and liver necrosis when treated with 300 and 500 mg/kg of APAP. C57BL/6 mice presented similar results only with 500 mg/kg of APAP. Our results show that A/J mice have a marked susceptibility to the effects of APAP and could be considered as an experimental model to study APAP-induced toxicity. (AU) | |
| Processo FAPESP: | 07/03393-2 - Expressão gênica dependente do componente C5 em fígado de camundongos com lesão hepática induzida por etanol |
| Beneficiário: | Lorena Bavia |
| Modalidade de apoio: | Bolsas no Brasil - Doutorado Direto |