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Neurotoxicity Research

, Volume 19, Issue 1, pp 49–54 | Cite as

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

  • Michela Russo
  • Stefania Cocco
  • Agnese Secondo
  • Annagrazia Adornetto
  • Antonella Bassi
  • Alfredo Nunziata
  • Giuliano Polichetti
  • Bruna De Felice
  • Simona Damiano
  • Rosalba Serù
  • Paolo Mondola
  • Gianfranco Di Renzo
Article

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 μg/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 μM). 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 μM). 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.

Keywords

Cigarette smoke condensate Antioxidant enzymes Vitamin E 

Notes

Acknowledgments

We are indebted to Dr. Anna Pannaccione, Division of Pharmacology, Department of Neuroscience, Federico II University of Naples and dr. Floriana Flamma, BAT Italia, for their valuable help. This study was partially supported by the grant PRIN 2007 to prof. Paolo Mondola.

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Copyright information

© Springer Science+Business Media, LLC 2009

Authors and Affiliations

  • Michela Russo
    • 1
  • Stefania Cocco
    • 1
  • Agnese Secondo
    • 1
  • Annagrazia Adornetto
    • 1
  • Antonella Bassi
    • 2
  • Alfredo Nunziata
    • 2
  • Giuliano Polichetti
    • 2
  • Bruna De Felice
    • 3
  • Simona Damiano
    • 4
  • Rosalba Serù
    • 4
  • Paolo Mondola
    • 4
  • Gianfranco Di Renzo
    • 1
  1. 1.Division of Pharmacology, Department of Neuroscience, School of Medicine“Federico II” University of NaplesNaplesItaly
  2. 2.Research and Development DepartmentBritish American Tobacco ItaliaRomeItaly
  3. 3.Department of Life ScienceSecond University of Naples (SUN)CasertaItaly
  4. 4.Division of Physiology, Department of Neuroscience“Federico II” University of NaplesNaplesItaly

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