Cigarette smoking condensate (CSC) contains oxidant compounds able to generate superoxide. The aim of the present study was to investigate the effect of the exposure to CSC on: (1) free radical production, (2) the gene expression of the antioxidant enzymes Cu-Zn superoxide dismutase (SOD1), Mn superoxide dismutase (SOD2), Glutathione Peroxidase (GPx), and catalase (CAT), and (3) cell survival in human neuroblastoma SH-SY5Y cells. The results showed that exposure (24 h) to different concentrations (10-150 mu g/ml) of CSC caused a dose dependent cell injury that was coupled to the maximal increase of free radical production. These events were prevented by the addition to the incubation medium of the scavenger Vitamin E (50 mu M). Furthermore, CSC exposure caused a reduction of the gene expression of the antioxidant enzymes SOD1, SOD2, GPx, and CAT that was counteracted by Vitamin E (50 mu M). These results suggest that CSC exposure can induce a free radical overcharge that may be responsible for the inhibition of antioxidant enzymes expression and cell injury in SH-SY5Y human neuroblastoma cells. In fact the scavenger vitamin E can block both cell injury and inhibition of SOD1, SOD2, GPx, and CAT induced by CSC exposure.

Cigarette Smoke Condensate Causes a Decrease of the Gene Expression of Cu-Zn Superoxide Dismutase, Mn Superoxide Dismutase, Glutathione Peroxidase, Catalase, and Free Radical-Induced Cell Injury in SH-SY5Y Human Neuroblastoma Cells

DE FELICE, Bruna;
2011

Abstract

Cigarette smoking condensate (CSC) contains oxidant compounds able to generate superoxide. The aim of the present study was to investigate the effect of the exposure to CSC on: (1) free radical production, (2) the gene expression of the antioxidant enzymes Cu-Zn superoxide dismutase (SOD1), Mn superoxide dismutase (SOD2), Glutathione Peroxidase (GPx), and catalase (CAT), and (3) cell survival in human neuroblastoma SH-SY5Y cells. The results showed that exposure (24 h) to different concentrations (10-150 mu g/ml) of CSC caused a dose dependent cell injury that was coupled to the maximal increase of free radical production. These events were prevented by the addition to the incubation medium of the scavenger Vitamin E (50 mu M). Furthermore, CSC exposure caused a reduction of the gene expression of the antioxidant enzymes SOD1, SOD2, GPx, and CAT that was counteracted by Vitamin E (50 mu M). These results suggest that CSC exposure can induce a free radical overcharge that may be responsible for the inhibition of antioxidant enzymes expression and cell injury in SH-SY5Y human neuroblastoma cells. In fact the scavenger vitamin E can block both cell injury and inhibition of SOD1, SOD2, GPx, and CAT induced by CSC exposure.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11591/217643
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