Phosphoinositide 3-kinase signaling in the cellular response to oxidative stress

2005 ◽  
Vol 386 (3) ◽  
Author(s):  
Andreas Barthel ◽  
Lars-Oliver Klotz
Keyword(s):  
Oxidative Stress ◽  
Cellular Response ◽  
Kinase Signaling ◽  
Phosphoinositide 3 Kinase

scholarly journals Cellular Response against Oxidative Stress, a Novel Insight into Lupus Nephritis Pathogenesis

2021 ◽  
Vol 11 (8) ◽  
pp. 693
Author(s):  
Corina Daniela Ene ◽  
Simona Roxana Georgescu ◽  
Mircea Tampa ◽  
Clara Matei ◽  
Cristina Iulia Mitran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lupus Nephritis ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
Control Group ◽  
Dna Repair Mechanisms ◽  
Glycation End Products ◽  
Repair Mechanisms ◽  
Low Levels ◽  
Defective Dna Repair

The interaction of reactive oxygen species (ROS) with lipids, proteins, nucleic acids and hydrocarbonates promotes acute and chronic tissue damage, mediates immunomodulation and triggers autoimmunity in systemic lupus erythematous (SLE) patients. The aim of the study was to determine the pathophysiological mechanisms of the oxidative stress-related damage and molecular mechanisms to counteract oxidative stimuli in lupus nephritis. Our study included 38 SLE patients with lupus nephritis (LN group), 44 SLE patients without renal impairment (non-LN group) and 40 healthy volunteers as control group. In the present paper, we evaluated serum lipid peroxidation, DNA oxidation, oxidized proteins, carbohydrate oxidation, and endogenous protective systems. We detected defective DNA repair mechanisms via 8-oxoguanine-DNA-glycosylase (OGG1), the reduced regulatory effect of soluble receptor for advanced glycation end products (sRAGE) in the activation of AGE-RAGE axis, low levels of thiols, disulphide bonds formation and high nitrotyrosination in lupus nephritis. All these data help us to identify more molecular mechanisms to counteract oxidative stress in LN that could permit a more precise assessment of disease prognosis, as well as developing new therapeutic targets.

Regulatory mechanisms of cellular response to oxidative stress

1999 ◽  
Vol 31 (4) ◽  
pp. 319-324 ◽  
Author(s):  
Ken Itoh ◽  
Tetsuro Ishii ◽  
Nobunao Wakabayashi ◽  
Masayuki Yamamoto
Keyword(s):  
Oxidative Stress ◽  
Cellular Response ◽  
Regulatory Mechanisms

scholarly journals Suppression of Phosphoinositide 3-Kinase Signaling and Alteration of Multiple Ion Currents in Drug-Induced Long QT Syndrome

2012 ◽  
Vol 4 (131) ◽  
pp. 131ra50-131ra50 ◽  
Author(s):  
Z. Lu ◽  
C.-Y. C. Wu ◽  
Y.-P. Jiang ◽  
L. M. Ballou ◽  
C. Clausen ◽  
...  
Keyword(s):  
Long Qt Syndrome ◽  
Ion Currents ◽  
Kinase Signaling ◽  
Long Qt ◽  
Drug Induced ◽  
Qt Syndrome ◽  
Phosphoinositide 3 Kinase

scholarly journals Evaluation of radical scavenging system in amoeba Chaos carolinense during nutrient deprivation

2017 ◽  
Vol 7 (4) ◽  
pp. 20160113 ◽  
Author(s):  
Yuru Deng ◽  
Edlyn Li-Hui Lee ◽  
Ketpin Chong ◽  
Zakaria A. Almsherqi
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Nucleic Acids ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
Antioxidant Activities ◽  
Radical Scavenging ◽  
Cellular Responses ◽  
Biological Macromolecules

The frequent appearance of non-lamellar membrane arrangements such as cubic membranes (CMs) in cells under stressed or pathological conditions points to an intrinsic cellular response mechanism. CM represents highly curved, three-dimensional nano-periodic structures that correspond to mathematically well-defined triply periodic minimal surfaces. Specifically, cellular membrane may transform into CM organization in response to pathological, inflammatory and oxidative stress conditions. CM organization, thus, may provide an advantage to cope with various types of stress. The identification of inducible membrane systems, such as in the mitochondrial inner membranes to cubic morphology upon starvation, opens new avenues for understanding the molecular mechanisms of cellular responses to oxidative stress. In this study, we compared the cellular responses of starved and fed amoeba Chaos carolinense to oxidative stress. Food deprivation from C. carolinense induces a significant increase in prooxidants such as superoxide and hydrogen peroxide. Surprisingly, we observed a significant lower rate of biomolecular damage in starved cells (with higher free radicals generation) when compared with fed cells. Specifically, lipid and RNA damages were significantly less in starved cells compared with fed cells. This observation was not due to the upregulation of intracellular antioxidants, as starved amoeba show reduced antioxidant enzymatic activities; however, it could be attributed to CM formation. CM could uptake and retain short segments of nucleic acids (resembles cellular RNA) in vivo and in vitro. Previous results showed that nucleic acids retained within CM sustain a minimal oxidative damage in vitro upon exposure to high level of superoxide. We thus propose that CM may act as a ‘protective’ shelter to minimize the oxidation of biologically essential macromolecules such as RNA. In summary, we examined enzymatic antioxidant activities as well as oxidative damage biomarkers in starved amoeba C. carolinense in correlation with the potential role of CM as an optimal intracellular membrane organization for the protection of biological macromolecules against oxidative damage.

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