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 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.
Phillips
J P
JP
Department of Molecular Biology and Genetics, University of Guelph, ON, Canada.
Campbell
S D
SD
Michaud
D
D
Charbonneau
M
M
Hilliker
A J
AJ
D000818:Animals; D002414:Cations, Monovalent; D003300:Copper / Q000633:toxicity; D004331:Drosophila melanogaster / Q000187:drug effects / Q000201:enzymology* / Q000235:genetics; D005260:Female; D007247:Infertility, Female / Q000235:genetics; D007248:Infertility, Male / Q000235:genetics; D008017:Life Expectancy; D008297:Male; D010269:Paraquat / Q000633:toxicity*; D013482:Superoxide Dismutase / Q000502:physiology*; D013481:Superoxides / Q000378:metabolism
D002414:Cations, Monovalent; D013481:Superoxides; D003300:Copper; D013482:Superoxide Dismutase; D010269:Paraquat