The effect of superoxide dismutase deficiency on zinc toxicity in Schizosaccharomyces pombe


TARHAN Ç., PEKMEZ M., KARAER UZUNER S., Arda N., TOPAL SARIKAYA A.

Journal of Basic Microbiology, cilt.47, sa.6, ss.506-512, 2007 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 47 Sayı: 6
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1002/jobm.200700220
  • Dergi Adı: Journal of Basic Microbiology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.506-512
  • Anahtar Kelimeler: Oxidative stress, Schizosaccharomyces pombe, Superoxide dismutase, Zinc toxicity
  • İstanbul Yeni Yüzyıl Üniversitesi Adresli: Evet

Özet

Zinc is a metal which is a cofactor in many enzymes and a structural element in zinc finger motifs those are important in relation between DNA and regulator proteins. Little is known about uptake, distribution, toxicity and detoxification of zinc ions in cells. In this study, zinc toxicity and detoxification levels have been compared in wild type and Cu/Zn superoxide dismutase mutant (sod1Δ) cells of the fission yeast Schizosaccharomyces pombe. We evaluated the toxic levels of zinc, total zinc content, lipid peroxidation levels and catalase activities for both strains which were grown in medium containing different concentrations of zinc. sod1‡ mutant showed important growth retardation and has higher lipid peroxidation and catalase activities than wild type. Cu/Zn superoxide dismutase (SOD1) activity of wild type cells was markedly increased when they were treated with elevated levels of zinc. SOD1 mRNA level also significantly increased when the cells treated with higher concentrations of zinc. These results indicate that the mutant cells were more sensitive to zinc stress and seemed to have more oxidative intracellular environment than wild type cells. Our results support the idea that superoxide dismutase is an important factor for zinc detoxification in eukaryotes. © 2007 Wiley-VCH Verlag GmbH & Co. KGaA.