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Proc Natl Acad Sci U S A. Apr 1989; 86(8): 2761–2765.
PMCID: PMC286998

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


The role of copper/zinc-containing superoxide dismutase (cSOD; superoxide:superoxide oxidoreductase, EC 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.

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