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Proc Natl Acad Sci U S A. 1989 Apr;86(8):2761-5.

Null mutation of copper/zinc superoxide dismutase in Drosophila confers hypersensitivity to paraquat and reduced longevity.

Author information

1
Department of Molecular Biology and Genetics, University of Guelph, ON, Canada.

Abstract

The role of copper/zinc-containing superoxide dismutase (cSOD; superoxide:superoxide oxidoreductase, EC 1.15.1.1) in metabolic defense against O2 toxicity in Drosophila is examined through the properties of a mutant strain carrying a cSOD-null mutation, cSODn108. Homozygotes are viable as larvae, which indicates that cSOD is not essential for cell viability per se. cSODn108 confers recessive sensitivity to the superoxide anion (O2-)-generator paraquat and to the transition metal compound CuSO4, which indicates that the cSOD-null condition in fact leads to impaired O2- metabolism. The primary biological consequences of the reduced O2- dismutation capacity of cSODn108 Drosophila are realized in the adult as infertility and reduction in life-span. We conclude that the infertility and reduced life-span of cSODn108 adults arise as a consequence of the reduced capacity of embryos, larvae, and pupae to adequately protect developing preimaginal cells from O2- -initiated cytotoxic damage.

PMID:
2539600
PMCID:
PMC286998
DOI:
10.1073/pnas.86.8.2761
[Indexed for MEDLINE]
Free PMC Article

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