Absence of electron transport (Rho 0 state) restores growth of a manganese-superoxide dismutase-deficient Saccharomyces cerevisiae in hyperoxia. Evidence for electron transport as a major source of superoxide generation in vivo

• Published in: The Journal of biological chemistry 1993-12, Vol.268 (35), p.26699-26703
• Main Authors: Guidot, D M, McCord, J M, Wright, R M, Repine, J E
• Format: Article
• Language: English
• Subjects: Electron Transport; Mitochondria - metabolism; Oxygen - metabolism; Saccharomyces cerevisiae - enzymology; Saccharomyces cerevisiae - growth & development; Saccharomyces cerevisiae - metabolism; Superoxide Dismutase - genetics; Superoxide Dismutase - metabolism
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1016/S0021-9258(19)74369-5

To address the possibility that electron transport is a biologically significant source of superoxide anion (O2-.) during exposure to hyperoxia in vivo, we constructed Saccharomyces cerevisiae strains with selective disruptions in the gene encoding the mitochondrial manganese-containing superoxide dismutase (Mn-SOD) and/or genes encoding proteins critical for complexes in electron transport. We hypothesized that complete absence of electron transport would restore growth in hyperoxia to a Mn-SOD-deficient yeast. We found that yeast deficient in Mn-SOD activity failed to grow normally in hyperoxia (95% O2, 5% CO2). In contrast, Mn-SOD-deficient yeast with complete absence of electron transport (the Rho 0 state) grew normally in hyperoxia. By comparison, Mn-SOD-deficient yeast which were deficient only in cytochrome-c-oxidase, the terminal step in electron transport, had only partially restored growth in hyperoxia. Our results indicate that electron transport is a major source of O2-. in vivo, and that the principal site of this O2-. production is proximal to the cytochrome-c-oxidase complex.