Research Output
Apoptosis induced by Paclitaxel, tobacco smoke condensate and hydrogen peroxide in lung epithelial cells (A549)
  Cigarette smoke is known to be a complex mixture of >4000 constituents dispersed between the volatile and non-volatile phase, and inhaled exposure causes lung inflammation and cell injury. Here we investigate the effects of some of components of cigarette smoke as inducers of apoptosis in A549 cells. Apoptosis is characterised by initial changes on the mitochondria, leading to chromatin condensation and ultimately DAM fragmentation. Cells were trated with 1um paclitaxel, 80ug/ml tobacco smoke condensate (TSC), 1uM nicotine and 10uM hydrogen peroxide for 24 and 48 hours. Attached and detached cells were stained with DAPI and visualised by fluoresence microscopy, % normal and apoptotic cells were determined. Results indicated morphological changes with time but quantification proved difficult. DNA was isolated and electrophoresed on 1% agarose gels. A DNA ladder was present in cells treated with paclitaxel, TSC and hydrogen peroxide but not nicotine. The presence of a DNA ladder indicates that late stage apoptotic events are occurring in these cells in exposure to certain components of tobacco smoke

  • Type:

    Meeting Abstract

  • Date:

    30 September 2004

  • Publication Status:

    Published

  • Publisher

    Springer Nature

  • DOI:

    10.1007/bf03353882

  • Cross Ref:

    BF03353882

  • ISSN:

    1023-3830

  • Library of Congress:

    QR180 Immunology

  • Dewey Decimal Classification:

    616 Diseases

  • Funders:

    University of Hertfordshire

Citation

Ramage, L., Jones, A., & Whelan, C. (2004). Apoptosis induced by Paclitaxel, tobacco smoke condensate and hydrogen peroxide in lung epithelial cells (A549). Inflammation Research, 53(S3), S207-S230. https://doi.org/10.1007/bf03353882

Authors

Keywords

Immunology, Pharmacology

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