Aluminium-induced DNA damage and adaptive response to genotoxic stress in plant cells are mediated through reactive oxygen intermediates

Mutagenesis. 2010 Mar;25(2):201-9. doi: 10.1093/mutage/gep063. Epub 2009 Dec 2.


Experiments employing growing root cells of Allium cepa were conducted with a view to elucidate the role of reactive oxygen intermediates (ROI) in aluminium (Al)-induced DNA damage, cell death and adaptive response to genotoxic challenge imposed by ethyl methanesulphonate (EMS) or methyl mercuric chloride (MMCl). In a first set of experiments, root cells in planta were treated with Al at high concentrations (200-800 microM) for 3 h without or with pre-treatments of dihydroxybenzene disulphonic acid (Tiron) and dimethylthiourea (DMTU) for 2 h that trap O(2)(.-)and hydrogen peroxide (H(2)O(2)), respectively. At the end of treatments, generation of O(2)(.-) and H(2)O(2), cell death and DNA damage were determined. In a second set of experiments, root cells in planta were conditioned by Al at low concentrations (5 or 10 microM) for 2 h and after a 2 h intertreatment interval challenged by MMCl or EMS for 3 h without or with a pre-treatment of Tiron or DMTU. Conditioning treatments, in addition, included two oxidative agents viz rose bengal and H(2)O(2) for comparison. Following treatments, root cells in planta were allowed to recover in tap water. Genotoxicity and DNA damage were evaluated by micronucleus (MN), chromosome aberration (CA) or spindle aberration (SA) and comet assays at different hours (0-30 h) of recovery. The results demonstrated that whereas Al at high concentrations induced DNA damage and cell death, in low concentrations induced adaptive response conferring genomic protection from genotoxic challenge imposed by MMCl, EMS and Al. Pre-treatments of Tiron and DMTU prevented Al-induced DNA damage, cell death, as well as genotoxic adaptation to MMCl and EMS, significantly. The findings underscored the biphasic (hormetic) mode of action of Al that at high doses induced DNA damage and at low non-toxic doses conferred genomic protection, both of which were mediated through ROI but perhaps involving different networks.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt / pharmacology
  • Aluminum Chloride
  • Aluminum Compounds / toxicity*
  • Astringents / toxicity*
  • Cell Death / drug effects
  • Chlorides / toxicity*
  • Chromosome Aberrations
  • Comet Assay
  • DNA Damage / drug effects*
  • Ethyl Methanesulfonate / toxicity*
  • Free Radical Scavengers / pharmacology
  • Hydrogen Peroxide / metabolism
  • Indicators and Reagents / pharmacology
  • Methylmercury Compounds / toxicity*
  • Mutagens / toxicity
  • Onions / drug effects*
  • Onions / growth & development
  • Oxidative Stress / drug effects
  • Plant Roots / drug effects
  • Plant Roots / growth & development
  • Reactive Oxygen Species / metabolism*
  • Superoxides / metabolism
  • Thiourea / analogs & derivatives
  • Thiourea / pharmacology


  • Aluminum Compounds
  • Astringents
  • Chlorides
  • Free Radical Scavengers
  • Indicators and Reagents
  • Methylmercury Compounds
  • Mutagens
  • Reactive Oxygen Species
  • Superoxides
  • Aluminum Chloride
  • 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt
  • 1,3-dimethylthiourea
  • Ethyl Methanesulfonate
  • Hydrogen Peroxide
  • Thiourea
  • methylmercuric chloride