Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to investigate the role of the Pap1 transcription factor in response to long-term Cd(2+) stress. The Schizosaccharomyces pombe wild-type strain and the Deltapap1 mutant, treated with 0.5 mM CdSO(4), were used in antioxidant enzyme and gene expression experiments. The Deltapap1 mutant proved to be sensitive to Cd(2+) in the spot test assay, suggesting that the Pap1 transcription factor plays an important role in the response to Cd(2+) stress. The Cd(2+) uptake was the same in both strains. Determination of the superoxide level in the wild-type strain proved that superoxide was generated, suggesting that long-term Cd(2+) treatment could trigger oxidative stress. Furthermore, the Deltapap1 mutant displayed higher amounts of superoxide. These results were supported by the significantly lower amount of peroxide generated in the reaction catalyzed by superoxide dismutase (SOD). The Deltapap1 mutant had a significantly lower glutathione S-transferase specific activity than that of the wild-type strain during long-term Cd(2+) stress, caused by the lower GSH and sulfide assimilation. We have demonstrated that GST III activity was not induced by Cd(2+) stress in the Deltapap1 mutant. The overall low GST activity was not sufficient for the cell to eliminate Cd(2+) caused damage and could result in a Cd(2+)-sensitive phenotype of the Deltapap1 mutant. The RT-PCR and Northern blot experiments proved that gst2 was not induced either by short-term or by long-term Cd(2+) treatment. The SPCC965.06 (a putative K(+) ion channel subunit) gene expression increased, while the hmt1 (an ABC-type vacuolar transporter protein) expression decreased in both strains. No detectable alteration in the mRNA levels of, gpx1, hmt2, sod1, sod, and trx1 was observed. SOD enzyme analyses revealed that the absence of Pap1 protein could result in a lower SODs activity and affect the sulfate assimilation. This is the first report on the fact that the Pap1 transcription factor could play an important role in the cellular post-transcriptional/post-translational enzyme activity induction processes of SODs that occur in response to Cd(2+).
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PMID:Gene expressions and enzyme analyses in the Schizosaccharomyces pombe Deltapap1 transcription factor mutant exposed to Cd(2+). 1730 22

Iron, a transition metal and essential nutrient, is a typical pro-oxidant forming free radicals, lipid peroxides and causing cell damage when added at high (> or = 50 microM) concentrations to oligodendroglia-like OLN-93 cells that have been enriched for 3 days with 10 microM docosahexaenoic acid (DHA, 22 : 6 n-3). At low (5 microM) iron concentrations lipid peroxides were still formed, but cells turned resistant to 250 microM H2O2, a secondary genotoxic stress. This has been attributed most likely to a time-dependent (16 h preconditioning) increase of cellular antioxidant enzyme activities i.e., glutathione peroxidase (38%) and glutathione reductase (26%). DHA but not arachidonic acid (20 : 4 n-6) supplements induced 3-fold increase in gene expression of divalent metal transporter-1, a transporter protein presumably responsible for the increase in intracellular iron. Elevated iron levels triggered a transient scrambling of membrane lipid asymmetry as evident by an accelerated ethanolamine phosphoglyceride translocation to the outer cell surface. Ethanolamine phosphoglyceride reorientation is proposed to activate certain signaling cascades leading to changes in nuclear transcription, a reaction that could represent a mechanism of preconditioning. These findings may have important implications for understanding the interactive role of iron and DHA in nutritional deficiencies, losses of polyunsaturated fatty acids in the aging brain or excessive iron accumulation in degenerative disorders.
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PMID:Docosahexaenoic acid-dependent iron accumulation in oligodendroglia cells protects from hydrogen peroxide-induced damage. 1820 40