Protective effects of bark ethanolic extract from Spondias dulcis Forst F. against DNA damage induced by benzo[ a] pyrene and cyclophosphamide

• Autor(a) principal: Araujo, Caroline de S.
• Data de Publicação: 2019
• Outros Autores: Brito, Lorrane D., Tarifa, Marina O., Farah da Silva, Nayara J., Rodrigues, Karoline S., Cavalcante, Dalita G. S. M. [UNESP], Gomes, Andressa S. [UNESP], Zocoler, Marcos A., Yoshihara, Eidi, Camparoto, Marjori L., Job, Aldo E. [UNESP], Kerche, Leandra E.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://dx.doi.org/10.1590/1678-4685-GMB-2018-0038; http://hdl.handle.net/11449/196334
• topic: Comet assay; micronucleus test; Spondias dulcis; cytotoxicity; mutagenicity

This study evaluated the genotoxicity, mutagenicity, antigenotoxicity, and antimutagenicity effects on biochemical parameters of oxidative stress of the Spondias dulcis bark ethanolic extract on mice. The extract was evaluated in the doses of 500, 1000, and 1500 mg/kg bw via gavage. To evaluate the protective effects of the extract, benzo[a] pyrene (B[a]P) and cyclophosphamide (CP) were chosen as DNA damage inducers. Genotoxicity and antigenotoxicity were evaluated by the comet assay. Cytotoxicity, mutagenicity, and antimutagenicity were evaluated by the micronucleus test in bone marrow and peripheral blood. The biochemical parameters of oxidative stress were evaluated by the quantification of catalase activity (CAT) and reduced glutathione (GSH) in total blood, liver and kidney, and malondialdehyde (MDA), in liver and kidney. No genotoxic, cytotoxic, or mutagenic effect was found on mice exposed to the extract. The extract depleted the number of damaged nucleoids in total blood and the number of micronucleus (MN) in both cell types. The extract was able to increase CAT activity and GSH levels and decrease MDA levels after treatment with B[a]P and CP. The results indicate that the S. dulcis extract has potential to be used as preventive compound against DNA damage caused by CP and B[a]P.