Authors: Phillips JP; Campbell SD; Michaud D; Charbonneau M; Hilliker AJ
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.
Keywords: Animals; Cations, Monovalent; Copper/toxicity; Drosophila melanogaster/drug effects/*enzymology/genetics; Female; Infertility, Female/genetics; Infertility, Male/genetics; Life Expectancy; Male; Paraquat/*toxicity; Superoxide Dismutase/*physiology; Superoxides/metabolism|
Journal: Proceedings of the National Academy of Sciences of the United States of America Volume: 86 Issue: 8 Pages: 2761-5 Date: April 1, 1989 PMID: 2539600 |
Phillips JP, Campbell SD, Michaud D, Charbonneau M, Hilliker AJ (1989) Null mutation of copper/zinc superoxide dismutase in Drosophila confers hypersensitivity to paraquat and reduced longevity. Proceedings of the National Academy of Sciences of the United States of America 86: 2761-5.
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