Disease relevance of Sod

• We tested the hypothesis that the Drosophila Cu,Zn SOD is capable of protecting Escherichia coli from oxidative damage caused by the herbicide paraquat [1].
• Phenotypic effects of familial amyotrophic lateral sclerosis mutant Sod alleles in transgenic Drosophila [2].
• This striking differential restoration of pleiotropic phenotypes could be the result of a threshhold of CuZnSOD expression necessary for normal male fertility and resistance to the toxicity of paraquat or hyperoxia which is lower than the threshold required to sustain a normal adult life span [3].
• The O. volvulus cytosolic and extracellular CuZnSOD genes (Ov-sod-1 and Ov-sod-2) are separated by 0.8 kb of sequence and are convergently transcribed [4].
• Our results show that, although the low-activity CuZnSOD allele of D. melanogaster confers hypersensitivity to paraquat, the near UV radiation damage was not affected [5].

Psychiatry related information on Sod

• There were no compensatory changes in the metabolic rate, level of physical activity, or the levels of other antioxidants, namely Cu-Zn SOD, catalase, and glutathione [6].

High impact information on Sod

• Altogether, these data show that increased expression of SOD1 is not required for the evolution of extreme lifespan, even in a system in which differential gene expression is the only way to express phenotypes with great lifespan differences [7].
• Moreover, interspecific comparisons show lower levels of antioxidant activities in longer-lived species, suggesting that life-span extension may evolve through less reactive oxygen species generation from the mitochondria rather than higher expression of SOD1 [7].
• The tremendous variation in lifespan between ant castes, ranging over 2 orders of magnitude, coupled with the fact that all individuals share the same genome, provides a system to investigate the role of SOD1 in the wild [7].
• Patterns of DNA sequence polymorphism at Sod vicinities in Drosophila melanogaster: unraveling the footprint of a recent selective sweep [8].
• The human wild-type and five FALS Sod mutant transgenes were introduced into the fruit fly, Drosophila melanogaster, in a Cu-Zn Sod null background [2].

Biological context of Sod

• Results from the present study indicate that elevated CuZn SOD activity, not Mn SOD, is the basis for the relatively high level of SOD activity in the chico (1) homozygotes [9].
• We have examined the patterns of polymorphism at two linked loci, Sod and Est-6, separated by nearly 1000 kb on the left arm of chromosome 3 of Drosophila melanogaster [10].
• At the Sod locus, a fairly strong (s>0.01) selective sweep, started >or=2600 years ago, increased the frequency of a rare haplotype, F(A), to about 50% frequency in populations of Europe, Asia, and the Americas [10].
• Genetic polymorphism at two linked loci, Sod and Est-6, in Drosophila melanogaster [10].
• FLP recombinase-mediated induction of Cu/Zn-superoxide dismutase transgene expression can extend the life span of adult Drosophila melanogaster flies [11].

Anatomical context of Sod

• The Cu-Zn SOD gene (Sod) cloned from Drosophila melanogaster was introduced via P element-mediated transformation into the germ line [12].
• Superoxide production by Drosophila mitochondria was measured fluorometrically as hydrogen peroxide, using its dependence on substrates, inhibitors, and added superoxide dismutase to determine sites of production and their topology [13].
• CuZn-SOD promoter-driven expression in the Drosophila central nervous system [14].

Associations of Sod with chemical compounds

• We also report that glutathione (GSH) depletion induced by administration of buthionine sulfoximine (BSO) selectively reduces the viability of mutants lacking CuZnSOD [15].
• Overexpression of Cu,Zn-SOD and catalase caused a retardation in the accumulation of 8-hydroxydeoxyguanosine during aging and in response to the exposure of live flies to x-rays [16].
• Copper-zinc superoxide dismutase appears to be a very erratic evolutionary clock [17].
• 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 [18].
• The gene for cytoplasmic superoxide dismutase (cSOD) maps within this interval, as does low xanthine dehydrogenase (lxd).--Recessive lethal mutations were generated within the region by ethyl methanesulfonate mutagenesis and by hybrid dysgenesis [19].

Other interactions of Sod

• Significant increases in the activities of both CuZn-SOD and catalase had no beneficial effect on survivorship in relatively long-lived y w mutant flies and were associated with slightly decreased life spans in wild type flies of the Oregon-R strain [20].
• This allowed us to confirm the results of (Clancy et al. 2001) and extend the results by measuring CuZn SOD and Mn SOD activities in addition to the previously determined overall SOD activity [9].
• I review the evolution of two genes, Gpdh and Sod [21].
• In addition, there are striking similarities to patterns of variation observed at the Est6 and Est-P loci, which are located approximately 1,000 kb from Sod [22].
• The combined data for three genes (Adh, Sod, and Gpdh) statistically resolves outstanding issues [23].

Analytical, diagnostic and therapeutic context of Sod

• Cloning, sequence analysis and chromosomal localization of the Cu-Zn superoxide dismutase gene of Drosophila melanogaster [24].
• One of the positive clones maps by in situ hybridization to position 68A8-9 on the left arm of polytene chromosome 3, the region to which cSOD mutants have previously been mapped genetically [25].
• We have developed a polyclonal antibody against synthetic SOD peptides that is specific for Drosophila CuZnSOD as shown by Western blots [26].

References