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 1.15.1.1) in metabolic defense against O2toxicity 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. cSODn108confers 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 cSODn108Drosophila are realized in the adult as infertility and reduction in life-span. We conclude that the infertility and reduced life-span of cSODn108adults arise as a consequence of the reduced capacity of embryos, larvae, and pupae to adequately protect developing preimaginal cells from O2 --initiated cytotoxic damage.