RESUMO
Tabebuia sp. is native to tropical rain forests throughout Central and South America. Although the biological and pharmacological effects of bark extracts have been intensely studied, little is known on the extract obtained from the flower. Herein, the genotoxic potential of a flower extract from T. impetiginosa ("ipê roxo") on the blood and liver cells of Wistar rats was evaluated. Experimental procedures involved only male animals. Graduated concentrations of the extract, viz., 100, 300 and 500 mg kg(-1) of body weight, were gavage-administered and 24 h latter cells were collected and processed for analysis. With the exception of the 100 mg kg(-1) dose, a significant increase in DNA damage was noted, when compared with a negative control group. Although the genotoxic potential of this extract was higher in liver cells, the response in both tissues was related to dose-dependency. Even though DNA damage can be corrected before conversion into mutations, further study is recommended to arrive at a better understanding of incurred biological effects.
RESUMO
To evaluate the incidence of chromosomal aberrations (CA) in peripheral lymphocytes of workers chronically exposed to chemical hazards in a tannery in Franca, São Paulo, Brazil. The exposed group consisted of 10 male workers employed in the same tannery. The duration of work in the tannery ranged from 5 months to 14 years. The control group consisted of 10 males without a history of exposure to chemicals or other potentially genotoxic substances. A total of 100 well-spread metaphases were analyzed per subject. The frequency of CA was higher in the exposed group than in the control group. Smoking had a significant effect on the frequency of CA in both the control and the exposed groups. Chronic occupational exposure of tannery workers represents a relevant risk factor for the development of diseases associated with genetic damage.
RESUMO
Lung epithelial cells are critical in the regulation of airway inflammation in response to environmental pollutants. Altered activation of NF-kappaB is associated with expression of several proinflammatory factors in respiratory epithelial cells in response to an insult. Here we show that a low threshold dose (8 microg/ml) of the jet fuel JP-8 induces in a rat alveolar epithelial cell line (RLE-6TN) a prolonged activation of NF-kappaB as well as the increased expression of the proinflammatory cytokines TNF-alpha and IL-8, which are regulated by NF-kappaB. The up-regulation of IL-6 mRNA in cells exposed to JP-8 appears to be a reaction of RLE-6TN cells to reduce the enhancement of proinflammatory mediators in response to the fuel. Moreover, lung tissues from rats exposed to occupational levels of JP-8 by nasal aerosol also showed dysregulated expression of TNF-alpha, IL-8, and IL-6, confirming the in vitro data. The poly(ADP-ribosyl)ation of PARP-1, a coactivator of NF-kappaB, was coincident with the prolonged activation of NF-kappaB during JP-8 treatment. These results evidenced that a persistent exposure of the airway epithelium to aromatic hydrocarbons may have deleterious effects on pulmonary function.