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1

The impact of toxic properties of oxygen on the evolution of life. II. Precambrian organisms and the origin of banded iron formations

100%
Bilinski T.
Bulletin of the Polish Academy of Sciences. Biological Sciences
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1988
|
tom 36
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nr 4-6
2
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EPR-spin labelling measurements of thylakoid membrane fluidity during barely leaf senescence

72%
Jajic I., Sarna T., Wisniewska A., Strzalka K.
BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology
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2013
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tom 94
|
nr 2
3

Reactive oxygen species [ROS] and reactive nitrogen species [RNS] alter metabolic effect of insulin in rat L6 satellite cells

58%
Orzechowski A., Grzelkowska K.
Polish Journal of Veterinary Sciences
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2000
|
tom 03
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nr 1
This study investigates the effect of superoxide anion radical (02); hydrogen peroxide (H202), nitric oxide (NO) and peroxynitrite (ONOO), which often accompany inflamed, endotoxic or exercised muscle on insulin action in DTsatellite cells. In order to induce quiescence, rat L6 myoblasts were subjected to transition from G2/M to Gl phase by the application of serum-reduced medium. Insulin stimulating effect on cell mitogenicity and anabolism was dose-dependent and hormetic. Application of H202 alone enhanced protein synthesis with dose-dependency but had no effect on mitogenicity. While insulin and H202 were used together, (i.e. at low H202 dose) insulin action was not affected regardless of the combination used, except the loss of dose- dependency on protein synthesis, but for 100 μM of H202 insulin action ceased abruptly and totally. Since there were no additive effects of both factors, we conclude that H202 may contribute to the insulin-induced anabolic reaction, however, below 100 The application of 02- donor stimulated protein synthesis and slightly inhibited [cell proliferation] though dose-response pattern was not observed suggesting apparent limitations to 02- diffusion into the cell. Moreover 02- inhibited both insulin-enhanced mitogenicity and protein synthesis by abrogating dose-response fashion of insulin action. The introduction of NO and ONOO- donors alone to control systems inhibited cell proliferation in a dose-dependent manner having no effect on protein synthesis (except the low doses of SIN-1). Insulin-stimulated syntheses of both DNA and protein were inhibited in a dose- dependent manner by SIN-1 (NO and 02' donor). In the presence of SNP (NO donor) mitogenic effect of insulin was abolished whereas protein synthesis was diminished only by the highest SNP concentration used (0.5 mM). Taken together, these results have shown that hydrogen peroxide (H202), nitric oxide (NO) and peroxynitrite (ONOO ) provide a good explanation for developing resistance to growth promoting activity of insulin in satellite cells under conditions of oxidant stress.
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