Acute crack cocaine exposure induces genetic damage in multiple organs of rats

• Autor(a) principal: Moretti, Eduardo Gregolin
• Data de Publicação: 2016
• Outros Autores: Yujra, Veronica Quispe, Claudio, Samuel Rangel, Silva, Marcelo Jose Dias [UNESP], Vilegas, Wagner [UNESP], Pereira, Camilo Dias Seabra, de Oliveira, Flavia, Ribeiro, Daniel Araki
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://dx.doi.org/10.1007/s11356-016-6141-3; http://hdl.handle.net/11449/172464
• topic: Crack cocaine; DNA damage; Genomic instability; Rat

Crack cocaine is a very toxic product derived from cocaine. The aim of this study was to evaluate genetic damage in multiple organs of rats following acute exposure to crack cocaine. A total of 20 Wistar rats were distributed into four groups (n = 5), as follows: 0, 4.5, 9, and 18 mg/kg body weight (b.w.) of crack cocaine administered by intraperitoneal route (i.p.). All animals were killed 24 h after intraperitoneal (i.p.) injection. The results showed that crack cocaine increased the number of micronucleated cells in bone marrow cells exposed to 18 mg/kg crack cocaine (p < 0.05). Peripheral blood and liver cells presented genetic damage as depicted by single cell gel (comet) assay at 9 and 18 mg/kg doses (p < 0.05). Immunohistochemistry data revealed significant increase in 8-hydroxy-20-deoxyguanosine (8-OHdG) immunoexpression in hepatocytes of animals exposed to crack cocaine at 9 and 18 mg/kg (p < 0.05) when compared with negative controls. Taken together, our results demonstrate that crack cocaine is able to induce genomic damage in multiple organs of Wistar rats.